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NCM 118 LEC
Care Of Clients With Life-Threatening Conditions, Acutely Ill / Multi-Organ Problems High
Acuity And Emergency Situation
LEC // PROF. SALAVANTE & PROF. DIZON
FINALS
○ Forceful expulsion of chyme from stomach
INTRODUCTION TO COMPLICATED GASTROINTESTINAL ■ Sometimes includes bile from
DISORDERS intestine
● Bulimia - Eating disorder
A. COMMON MANIFESTATIONS OF DIGESTIVE SYSTEM ○ DamagetostructuresoftheGltractcaused
DISORDERS by recurrent vomiting
● Health History - get a good history taking byasking ■ Oral mucosa
focus questions on the following: ■ Teeth
○ Appetite ■ Esophagus
○ Food intolerance ○ Don’t ask directly but ask about food
○ Weight-gain/loss patterns, intolerance, activities, even
○ Dysphagia emotionalaspectsthatmightbeaffectingthe
○ Nausea px’s metabolism(includeADLandGordon’s
○ Vomiting Pattern of Functioning)
○ Regurgitation
○ Dyspepsia Characteristics of Vomitus:
○ Heartburn
○ Pain ● Presence of blood - Hematemesis
○ Constipation ○ Coffee ground vomitus-brown granular
○ Diarrhea material indicates action of HCI on
○ Jaundice hemoglobin
○ Stool changes ○ Hemorrhage - red blood may be in vomitus
● Yellow or green-stained vomitus
Anorexia, Nausea, Vomiting, and Bulimia: ○ Bile from the duodenum
● Deeper brown color
● hisisverycommon,soaskforcues(e.g.whythepx
T ○ May indicate content from lower intestine
is having vomiting episode, and why are they ● Recurrent vomiting of undigested food
nauseated) ○ Problem with gastric emptying or infection
● May be signsofdigestivedisorderorothercondition
elsewhere in the body Bristol Stool Chart:
○ Systemic infection
○ Uremia
● ype 1 - Separate heard limps (severe constipation)
T
○ Emotional responses ● Type 2 - Lumpy and sausage like (mild constipation)
○ Motion sickness ● Type 3 - A sausage with cracks in the surface
○ Pressure in the brain (normal)
○ Overindulgence of food,drugs ● Type 4 - Like a smoore soft sausage or snake
○ Pain (normal)
● Associate manifestation, synthesize, and correlate
● Type 5 - Soft blobs with clear cut edges (lacking fiber)
with whatever condition the patient has ● Type 6-Mushyconsistencywithraggededges(mild
● Anorexia and Bulimia diarrhea)
○ Ask about eight, if gained or lost some ● Type7-Liquidconsistencywithnosolidparts(severe
○ Anyformofactivities/eventsthatleadtothe diarrhea)
lost or gaining of weight ○ Patientmayhidesomethingfromtheirhealth
○ when talking about metabolism, we wantto history so add observation to the technique
look at the px in a bigger picture ○ Engages senses in assessing the stool,
● Anorexia and vomiting otherwise, assessment is incomplete
○ Can cause serious complications:
Dehydration, acidosis, malnutrition Diarrhea:
● Anorexia
○ Often precedes nausea and vomiting ● Excessive frequency of stools
● Nausea ○ Usually of loose or watery consistency
○ Unpleasant subjective feeling
● May be acute or chronic
○ Simulated by distention, irritation, ● Frequently with nausea and vomiting when infection
inflammation of digestive tract or inflammation develops
○ Also stimulated by smells, visual images,
● May be accompanied by cramping pain
pain, and chemical toxins and/or drugs ● Prolonged diarrhea may lead to dehydration,
● Vomiting (Emesis) electrolyte imbalance, acidosis, malnutrition
○ Vomiting center located in the medulla ● Askaboutstoolpatter(numberoftimes,consistency,
■ Coordinates activities involved in characteristic, odor)
vomiting ● During episode of diarrhea, is there pain?
■ Protects airway during vomiting
1
● ssociatewitheffectseg.leadingtodehydrationand
A
○ bdominal distention and pain
A
electrolyte imbalance ○ Flatus
Common Types of Diarrhea: Constipation:
● Large-volume diarrhea (secretory or osmotic) ● Less frequent bowel movements than normal
○ Watery stool resulting from increased ○ There is pain on defacation
secretions into the intestine from the plasma
● Small hard stools
○ Often related to infection ● Acute or chronic problem
○ Limited reabsorption because of reversalof ● May be caused by decreased peristalsis
normal carriers for sodium and/or glucose ○ Increased time for reabsorption of fluid
○ No reabsorption of sodium and glucose ● Periods of constipation may alter with periods of
○ Associated with infection diarrhea.
● Small-volume diarrhea ● Chronic constipation may cause hemorrhoids, anal
○ Often caused by inflammatory bowel disease fissures, or diverticulitis.
○ Stool may contain blood, mucus, pus
● Very common in acute inflammatory bowel disease
○ May be accompanied byabdominalcramps ● Can also be from decreased peristalsis
and tenesmus ● Influenced by the dietary intake and fluid intake
○ Tenesmus-feelingthatyouneedtodefecate
but there is none. Alsofeelrectalpain,and Causes of Constipation:
straining but still, there is none
● Steatorrhea - "fatty diarrhea" ● eakness of smooth muscle because of age or
W
○ Frequent bulky, greasy, loose stools illness
○ Foul odor
● Inadequate dietary fiber
○ Characteristic of malabsorption syndromes ● Inadequate fluid intake
■ Celiac disease, cystic fibrosis ● Failure to respond to defecation reflex
■ LIVER DISEASEas well ● Immobility
○ Fat usually the first dietary component ○ Why we encourage passive
affected movement/exercise for critical patients
■ Presence interferes with digestion ○ For ambulatorypatient,weencouragetodo
of other nutrients. simple exercise as simple as walking
○ Abdomen often distended ○ Immbolity lessens peristalsis
● Neurological disorders
Blood in Stool: ● Drugs (i.e., opiates)
○ Some antacids, iron medications
● lood may occur in normal stools with diarrhea,
B ● Obstructions caused by tumors or strictures
constipation, tumors, or an inflammatory condition.
○ Frank blood Fluid and Electrolyte Imbalance:
■ Red blood-usually from lesions in
rectum or anal canal
● specially if vomiting or having diarrhea
E
○ Occult blood ● Assess what are the manifestations coming from a
■ Small hidden amounts, detectable decrease of a particular electrolyte
with stool test ● Weneedtobecarefulinassessingthemanifestation
■ May be caused by small bleeding so we can rule out and diagnose appropriately and
ulcers know if it is GIT in origin
■ It is tested - undergo FECAL ● Dehydration and hypovolemia are common
OCCULT BLOOD TEST (FOBT) complications of digestive tract disorders.
● NOTE: Px should be in ● Electrolytes
meat-free diet in order for ○ Lost in vomiting and diarrhea
the Medtech to see is ● Acid-base imbalances
there is occult blood ○ Metabolic alkalosis
○ Melena ■ Results from loss of hydrochloric
■ Dark-colored, tarry stool acid with vomiting
■ Mayresultfromsignificantbleeding ● Metabolic acidosis
in upper digestive tract ○ Severe vomiting causes a change to
○ Hematochezia metabolic acidosis because of the loss of
■ Fresh blood in stool bicarbonate of duodenal secretions.
● Take a look if fresh, tarry stool, or occult blood ○ Diarrhea causes loss of bicarbonate.
● Especiallyincaseofliver/hepaticcase,becarefuland
characterizing. Spread the stool in the diaper to check Pain: Visceral Pain:
Gas: ● Burning sensation
○ Inflammation and ulceration in upper
● rom swallowed air, such as drinking from a straw
F digestive tract
● Bacterial action on food ● Dull, aching pain
● Foods or alterations in motility ○ Typical result of stretching of liver capsule
● Excessive gas causes: ● Cramping or diffuse pain
○ Eructation / Belching ○ Inflammation, distention, stretching of
○ Borborygmus intestines
2
● Colicky, often severe pain
○ Recurrent smooth muscle spasms or ramping
C iliary colic, Irritable bowel
B
contraction (Namimilipit/Pinipiga) syndrome, Diarrhea,
■ Response to severe inflammation Constipation, Flatulence
or obstruction
Severe Cramping ppendicitis, Crohn's
A
Pain: Somatic Pain: Disease, Diverticulitis
● Somatic pain receptors directly linked to spinal nerves Stabbing Pancreatitis, Cholecystitis
○ May cause reflex spasm of overlying
abdominal muscles
● Steady, intense, often well-localized abdominal pain Malnutrition:
● Involvement or inflammation of parietal peritoneum
● Rebound tenderness-identified over area of ● ecanseeasanendresult,especiallyifthereisno
W
inflammation when pressure is released absorption of nutrients at all
● May be limited to a specific nutrient or general
Pain: Referred Pain: ● Causes of limited malnutrition-specific problem
○ Vitamin B12 deficiency
● alk about the origin of pain
T ○ Iron deficiency
● Most of the organs are not visible. Pain associated ● Causes of generalized malnutrition
with one organ can have a referred pain ○ Chronic anorexia, vomiting, diarrhea
● Common phenomenon ○ Other systemic causes
● Pain is perceived at a site different from origin. ■ Chronic inflammatory bowel
● Results when visceral and somatic nervesconverge disorders
at one spinal cord level ■ Cancer treatments
● Source of visceral pain is perceivedasthesameas ■ Wasting syndrome
that of the somatic nerve. ■ Lack of available nutrients -
● May assist or delay diagnosis, depending on problem common in poor countries (e.g.
● Pancreatitis - expect there is back pain radiating Sumalia)
upward
● Biliary colic - pain in the back B. UPPER GASTROINTESTINAL TRACT DISORDERS
● Appendicitis - pain in McBurney’s point
● Liver problem - pain on the right, upward Stress Ulcer:
● Associated with severe trauma or systemic problems
○ Burns, head injury
○ Hemorrhage or sepsis
● Rapid onset
○ Multiple ulcers (usually gastric) may form
within hours of precipitating event
○ First indicator-hemorrhage and severe pain
● Usually complain of bleeding or severe pain
● Need to go back in PUD
● Affected how the body responses so stress, be it
pathologic or simply stress in nature.
● Your body responds hyperactively so the stomach
produces moregastricacidinresponsetothestress
level leading to stress gastritis and from stress
gastritis leading to stress ulcer
● Have a lot oflimitations.Onethingthatshouldbein
place is CONTROL. Control the stress level
○ Eliminate the source of stress
○ Look into the underlying cause (e.g. if
emotional then do emotional intervention)
○ Eliminate a lot of food in your diet )e.g.
coffee, tea, chocolate, sweet, salty, too
much fat) because these can trigger an
attack
Dumping Syndrome:
● ollection of manifestation
C
● Control of gastric emptying is lost, and gastric
contents are "dumped" into the duodenum without
ABDOMINAL PAIN POSSIBLE CAUSE complete digestion.
HARACTERISTIC
C
● May follow gastric resection
● Hyperosmolar chyme draws fluid from vascular
Burning (Mahapdi) Peptic ulcer, GERD compartment into intestine
○ Intestinal distention
3
○ Increased intestinal motility ○ Inflammation and pain may temporarily
○ Decreased blood pressure → anxiety and subside.
syncope ● Localized infection orperitonitisdevelopsaroundthe
● Complicationinpxwhounderwentgastrectomy/ total appendix.
gastrectomy ○ May spread along the peritoneal membranes
○ (3) Incomplete gastric emptying it goes ● Increased necrosis and gangrene in the wall
directly to the smallintestinewithoutproper ○ Caused by increasing pressure in the
digestion appendix
● Appendix ruptures or perforates
○ Release of contents into peritoneal cavity
○ Generalized peritonitis
■ May be life-threatening
● Treatment
○ Surgical removal of appendix and
antimicrobial drugs
● Occurs during or shortly after meals
○ Abdominal cramps, nausea, diarrhea
● Hypoglycemia 2 to 3 hours after meal
○ Highbloodglucoselevelsinchymestimulate
increased insulin secretion → dropinblood
glucose levels
● May be resolved by dietary changes
○ Frequent small meals-highinprotein,lowin
simple carbohydrates
○ Position px properly Appendicitis: Signs and Symptoms
● Often resolves over time
● Hypoglycemiainprolongedperiodisnotgoodforthe ● General periumbilical pain
metabolic processes ○ Related to the inflammation
● Nursing Consideration:
● Nausea and vomiting common
○ avoid CHO/sweets ● Pain becomes severe and localized in lower right
○ increased fat and CHON, decrease CHO quadrant (LRQ).
○ six small dry meals ● LRQ rebound tenderness develops.
○ no fluidsaftermeal,mayhavefluids2hrs ○ Involvement of parietal peritoneum over
after meals appendix
○ lie supine after meal 1/2 hr ● After rupture
■ allows proper digestion ○ Pain subsides temporarily.
■ should not be at risk for aspiration ● Painrecurs-severe,generalizedabdominalpainand
○ avoid fowlers position after meal guarding
○ Once it has spilled its content into the
C. LOWER GASTROINTESTINAL TRACT DISORDERS peritoneal area
● Low-grade fever and leukocytosis
Appendicitis: Development ○ Development of inflammation
● Boardlike abdomen, tachycardia, hypotension
● oesn’t expose to a high risk condition, but if it
D ○ As peritonitis develops, abdominal wall
evolves to more inflamed appendix, then you are muscles spasm.
prone to have ruptured appendix which is a serious ○ Toxins lead to reduced blood pressure.
problem in 24-48 hours ● Other signs of Inflammation
● Obstruction of the appendiceal lumen ○ Psoas signis pain on hip flexion
○ By a fecalith, gallstone, or foreign material ○ Obturatorsignispainoninternalrotationof
● Fluid builds up inside the appendix. the hip
○ Microorganisms proliferate ○ Rovsing's sign is pain on the right side
● Appendiceal wall becomes inflamed. when pressing on the left
○ Purulent exudate forms ■ Maybeelicitedbypalpatingtheleft
○ Appendix is swollen. lower quadrant; this paradoxically
● Ischemia and necrosis of the wall causes pain to be felt at the right
○ Results in increased permeability lower quadrant.
● Bacteria and toxins escape into surroundings. ● Psoas & Obturator sign
○ Leads to abscess formation or localized ○ Painelicitedbyeitherthepsoasorobturator
bacterial peritonitis maneuvers suggests irritation of the
● Abscess may develop when inflamed area iswalled respective muscles by an inflammatory
off. process such as acute appendicitis, a
4
ruptured appendix or pelvic inflammatory ○ nce there is deverticulosis, fecesdointoit
o
isease (PID).
d causing inflammation
● McBurney's Point is ontheabdominalwallthatlies ○ inflammation cand lead to rupture
betweenthenavelandtherightanteriorsuperioriliac ○ onceitruptures,thecontent(feces)canspill
spineandthatisthepointwheremostpainiselicited into the peritoneal cavitty leading to
by pressure in acute appendicitis PERITONITIS
● Form at gaps between muscle layers
● Congenital weakness of wall may be a factor
● Weaker areas bulge when pressure increases.
● Many cases are asymptomatic.
● Diverticulitis stasis of material in diverticula leads to
inflammation and infection.
○ Cramping, tenderness, nausea, vomiting
○ Slight fever and elevated white blood cell
count
● Treatment of diverticulitis
○ Antimicrobial drugs
○ Dietary modifications to prevent stasis
● Medical Management
○ Diet
Appendicitis: Management ■ Initial: Clear Liquid
■ Subsequent: High fiber low fat diet
● emi fowler's to relieve pain and discomfort
S ■ Acute Infected Diverticulitis: low
● NPO fiber diet
● No pain relievers ■ Increase oral fluid intake
○ we are evaluating pain. we will be blind to ○ Medication
the patient’s status (if the appendix has ■ Antibiotics
ruptured already) ■ Antispasmodics
● No laxatives and enemas as it may rupture ■ Opioids
● No warm compress ○ Hospitalization (if required)
○ it might trigger rupture and can progress ○ Surgical Management
severely ■ One-stage resection
● NGT insertion ■ Two-stage resection
■ Dependonthesituationofthelarge
Appendicitis: Surgery (Appendectomy) intestine
● Surgery - removal of the appendix
○ Classic - a standard small incision in the
rightlowerpartoftheabdomen(McBurney's
incision)
○ Laparoscopy - requires 3 to 4 small incision
● Complications:
○ Rupture
○ Peritonitis and abscess
○ Organ failure and death
Diverticular Disease
● evelopment of diverticula
D
● Diverticulum
○ Outpouching (herniation) of the mucosa
through the muscular layer of the colon
○ the pathogenesis lies on the weakened
mucosal layer of the large intestine,
outpouching or herniation happens
● Diverticulosis
○ the outpouching
○ Asymptomatic diverticular disease
● Diverticulitis
○ when the outpouching inflames
○ Inflammation of the diverticula Diverticular Disease: Hartmann’s Procedure
● Asymptomatic if controlled, but if there’s too much
pressure pushing the weakened walls of the large ● proctosigmoidectomy, Hartmann's operation or
A
intestine, the diverticula can expand insizeandcan Hartmann'sprocedureisthesurgicalresectionofthe
be inflamed leading to diverticulitis rectosigmoid colon with closure of the anorectal
● Why is it complicated: stumpandformationofanendcolostomy.Itwasused
○ weakened large intestine to treat colon cancer or inflammation
○ large intestine carries feces (proctosigmoiditis, proctitis, diverticulitis, etc.).
5
● heportionthatisnotfunctionalwillberemoved,and
T ○ ehydration, hypovolemia, low blood
D
then create a passage where the stool can pass pressure
through. ○ Decreased blood pressure, tachycardia,
● There is a total closure of the distal stump fever, leukocytosis
● Treatment
○ Depends on primary cause
■ itisacomplicationofmanyformsof
GIT disorders
○ Surgery might be required.
○ Massive antimicrobial drugs specific to
causative organisms
Diverticular Disease: Nursing Management
● ssessment of dietary habits, signs and symptoms
A
such as straining, constipation, tenesmus, diarrhea,
bloating, and distention
● Maintaining Normal Elimination Patterns
○ Increasing oral fluid intake to up to 2L/day
○ High fiber diet
○ Bulk laxatives, stool softener, oil retention
enema D. ACCESSORY ORGANS
■ we do not use laxative AT ALL,
howeveritwillbeonacasetocase Chronic Liver Disease
basisbecauseofthepossibilitythat
it can aggravate ● lcohol takes the top of the survey in developing
A
● Pain Relief Chronic Liver Disease
● Analgesics, Antispasmodics ● A lot of things can be initiating chronicliverdisease
● Educateclienttoavoidactivitiesthatexertstoomuch from lifestyles, stress, certain meds, diet fatty foods
intra-abdominal pressure
● Not just alcohol causing it
● Progressive destruction of the liver
Peritonitis
Causes:
● Inflammation of the peritoneal membranes ● Alcoholic liver disease (alsoknownasLynixdisease
● Chemical peritonitis may result from: or Lynix cirrhosis)
○ Enzymes released with pancreatitis ○ Most common cause
○ Urine leaking form a ruptured bladder ● Biliary cirrhosis
○ Chyme spilled from a perforated ulcer ○ Associated with immune disorders
○ Bile escaping from the ruptured gallbladder ● Postnecrotic cirrhosis
Blood ○ Linked with chronic hepatitis or long-term
○ Any other foreign material in the cavity exposure to toxic materials
● Bacterial peritonitis caused by: ● Metabolic
○ Direct trauma affecting the intestine ○ Usuallycausedbygeneticmetabolicstorage
Ruptured appendix disorders
○ Intestinal obstruction and gangrene
● Any abdominal surgery Cirrhosis
○ If foreign material is left or infection develops
● Pelvic inflammatory disease in women ● Extensive diffuse fibrosis
○ When infection reaches the cavity through ○ Fibrotic changes interferes with blood supply
fallopian tubes ○ Bile may back up.
● In peritonitis there is boardlike rigid abdomen
● Loss of lobular organization
● increased permeability exposes the whole cavity to ● Degenerative changes may be asymptomatic until
the accumulation ofbacteria.bacterialperitonitiscan disease is well advanced.
develop abscess ● Liver biopsy and serologic test to determine cause
● obstruction will cause problems in peristaltic and extent of damage
movement, abscess can trigger infection and ● Doctor may order liver biopsy and serologic test to
developing septic shock determine the cause and the extent of the chronic
● Signs and symptoms liver disease
○ Sudden, severe, generalized abdominal pain
○ Localized tenderness at site of underlying Cirrhosis: Alcoholic Liver Disease
problem
○ Vomiting common, abdominal distention ● Initial stage -fatty liver
6
○ nlargement of the liver
E ■ Increased urobilinogen = Dark
○ Asymptomatic and reversible withreduced orange urine
alcohol intake ● Liver fibrosis and scarring
○ It istreatableandpreventable,exerciseand ○ Portal hypertension
proper diet can decrease fatty liver ■ Edema, esophageal varices,
○ If alcohol is not controlled, and no ■ hemorrhoids, caput meducae,
modification in lifestyle, can develop stage 2 ascites
● Second stage-alcoholic hepatitis ■ Splenomegaly = ANEMIA
○ Inflammation and cell necrosis ■ Thrombocytopenia, Leukopenia
○ Fibrous tissue formation-irreversible change ● Bleeding, Delayed Wound
○ Once liver is damaged IT IS IRREVERSIBLE Healing, Infection
○ Onceitstartstransformingintofibroustissue ● Liver failure
formation, it is irreversible. ○ Inability to metabolize ammonia to urea
○ That is why many people die with liver ■ Increased serum ammonia, Fetor
dieases,thediseaseisnotcurableinitsend hepaticus
stage ○ Hepatic encephalopathy
● Third stage-end-stage cirrhosis ■ Asterixis, Respiratory Acidosis,
○ Fibrotic tissue replaces normal tissue Sleep Alteration, Decreased LOC
○ Little normal function remains ○ Hepatic coma
● As liver damage progresses, it converts into fibrous ■ Death
tissue ● Very complex,multitudeofprocessesthatintheend
● If it converts into fibrous tissue, liver function will lead to liver failure
decreases as it converts into a hard edge liver
● In metabolism, emphasis on function of liver
● Ifliverisnotgood,whowilldoalotofsynthesisand
metabolic process, the px will suffer a lot. It is a
multitude of effects
● When it gets worse, it is irreversible
Cirrhosis: Pathophysiology with Signs and Symptoms
● omplexdisordersbecauseitcoversalotofdisease
C
within a disease entity
● Liverinsult,alcoholingestion,viralhepatitis,exposure
to toxins
● Hepatocyte damage
● Liver inflammation
○ Increased WBC
○ Fatigue, N/V, Pain, Fever, Anorexia
● Alterations in blood and lymph flow Jaundice
● Liver necrosis
○ Decreased ADH and aldosterone ● ellow discoloration of the skin because of the
Y
detoxification accumulation of bilirubin pigment
■ Edema ● Increased
○ Decreased androgen, and estrogen ○ Bilirubin Direct >.1-.3mg/dl
■ Palmarerythema,testicularatrophy, ○ Indirect >.2-.7 mg/dl
spider angiomas, gynecomastia,
● A symptom of a disease
loss of body hair, menstrual ● Yellow pigmentation of the skin
changes ● Due to accumulation of bilirubin pigment
○ DecreasedmetabolismofCHO,CHON,and ● Usually observed first in the sclera (Icteresia)
Fats ● Kernicterus (brain) fatal
■ Ascites,Edema,Hypoglycemiaand ○ Most fatal form
Malnutrition, Steatorrhea ● When jaundice appears, it is because of too much
○ Decreased Vitamin K absorption destruction of RBC through increasing bilirubin
■ Bleeding tendency ● Clinical Manifestation:
○ Decreased bilirubin metabolism ○ deep orange, foamy urine
■ Hyperbilirubinemia = Jaundice ○ dark tea-colored urine
■ Decreased bile in GIT = Clay ○ clay-colored stool
colored stool ○ severe itchiness-bile salts
○ steatorrhea
● Control pruritus
7
○ alamine lotion
c ● emove 1-1.5L of fluid
R
○ baking soda with caution
○ NaHCO3 ● Nursing Consideration:
○ Antihistamine ○ Monitor nutrition
○ Soothing baths ■ Modify diet
● Drug ■ Restrict sodium (200-500mg/day)
○Cholestyramine - it binds bile salts in the ■ Restrict fluids (1000-1500 ml/day)
intestine and eliminated via feces. High calorie diet
● Look for the cause and manage it ○ Prevent increasing edema
○ Start preventingliverinsultbymodifyingthe ■ Administer diuretics as ordered
lifestyle because once liver is inflamed, it’s ■ Monitor I and O
irrversible ■ Measure abdominal girth
■ Adminster salt poor albumin to
Portal Hypertension replace vascular volume (dextran
70, Haemaccel)
● aused by portal vein obstruction
C
● Clinical Manifestations Esophageal Varices
○ esophageal varices,umbilicalvarices(caput
medusae), hemorrhoids
● ilatation of the veins of esophagus
D
○ fluid extravasation ● Resulting in distension, hypertrophy, increase fragility
○ ascites and edema ● It is because of the portal hypertension
● ↑ Collateral circulation ● Once it ruptures, it bleeds
○ Px is having liver necrosis and liver fibrosis ● Liverfailurehavebleedingproblems,sotherewillbe
○ hemorrhoids problem with the platelets and the stopping of the
○ spiderangioma (dilated vessels w/d red bleeding if the varices rupture
○ palmar erythema (inc Estrogen) ● Assessment:
○ esophageal varices ○ Anorexia, N&V, hematemesis, fatigue,
○ center) weakness
○ Splenomegaly, ascites,caput medusae,
peripheral edema
● Medical management
○ Iced normal saline lavage
○ Transfusion with FWB
○ Vit. K
○ Sengstaken Blakemore tube (3 lumen)
■ Importantinstrumentatpxbedside:
Scissors (if there is bleeding, and
you need to stop the bleedingand
decompress, you need to cut
through to relieve from possible
aspiration)
○ Injection sclerotherapy
■ Prevent bleeding and rupture
● Surgery
○ Ligation of esophageal varices
■ Rubber band ligation done
endoscopically
Ascites ○ Surgery for portal HPN
● Promote comfort
● ccumulation of free fluids in the peritoneum
A ● Monitor for further bleeding and signs of shock
● Assessment: P.E reveals fluid wave, shifting dullness ● Health teaching
● Increasing amount of fluids between the abdominal ○ Minimizing esophagealirritation(avoidASA,
structure that’s why there’s abdominal alcohol)
distention/enlargement ○ Avoid increased abdominal thoracic pressure
● Medical management: Supportive: ○ Report signs of hemorrhage
○ Modify diet
● It depends on the status of the liver
○ Bed rest ● To control varices, then control portal HPN, this is
○ Albumin irreversible
● Diuretic Therapy ● Nursing Considerations:
● Surgery - fluid in the peritoneum is drained through ○ Monitor pt with Sengstaken Blakemore tube
paracentesis ■ Facilitate placement of tube
○ Paracentesis - assessed for cell count, ■ Prevent dislodgment bypositioning
specific gravity, protein, microorganisms (semi- fowlers)
■ Indicated for respiratory and ■ Keep scissors at bedside at all
abdominal distress times
● Empty bladder before ■ Monitor Respiratory status: if
procedure distress occurs cut the tube to
● Monitor BP for signs of deflate and remove tube
hypotension
8
● Ifbleedingcontinues,pxis
at risk for aspiration and DANGEROUS
also have an aggravated
respiratory status and 4 omatose; may not
C bsence of asterixis;
A
develop respiratory respond to painful absenceofdeeptendon
distress stimuli (or any stimulus reflexes; flaccidity of
■ Care of nares to avoid cracking at all) extremities. EEG
■ Label each lumen, maintain markedly abnormal.
prescribed amount of pressure of
esophageal balloon and deflate as
● iagnostics test: Serum ammonia Level
D
ordered to avoid necrosis ● Nursing Considerations:
○ Frequentneuroassessmentwithemphasisif
the patient is detriorating from time to time
○ Conduct neurologic assessment, report
deterioration
○ Restrict protein in Diet. High CHO, Vit. K
○ Administer enemas, cathartics intestinal
antibiotics and lactulose
■ Want the pt to defecatemorethan
3x or 4x or more becausethrough
this ammonia is excreted
○ Protect pt from injury
○ Avoid hepatotoxic drugs (acetaminophen,
phenothiazines)
○ Bed rest
Hepatic Encephalophalopathy ● Drugs
○ Neomycin (bacterial flora responsible for
● iver unable to convert ammonia to urea causing
L NH4 production)
neurologic symptoms ○ Lactulose (promote excretion of NH4 and
● Assess for changes in mental function. cause osmosis decreasing stool transit time)
● The disease progresses and the last part of the ■ Limit pt meds simply becauseliver
disease process is not functioning well. Provide IV
● Aggravated by GI bleeding drugs, or put in NPO and convert
● Assessment: oral drugs to IV drugs
○ Change of mental function (irritability,
insomnia, slight tremor slurred speech, Acute Pancreatitis
babinski reflex, hyperactive reflexes)
○ Progressive disease (asterixis, ● Inflammation of the pancreas
disorientation, apraxia, tremors, fetor ○ Results inautodigestionof the tissue
hepaticus) ○ Autodigestion - the enzymes digest the
○ Late manifestation of the disease (Coma, pancreas itself. Destroys thesurroundingof
absent reflexes) pancreas leading to necrosis of tissue and
inflammation
● May be acute or chronic
○ Acute form considered a medical emergency
● Pancreas lacks a fibrous capsule
○ Destruction may progress into tissue
Stage Clinical Symptoms Clinical Signs and surrounding the pancreas
EEG Changes ○ Substancesreleasedbynecrotictissuelead
to widespread inflammation
1 ormal
N level of sterixis;
A impaired ■ Hypovolemia and circulatory
consciousness with writing and ability to collapse may follow.
periods of lethargy and draw line figures. ● Chemical peritonitis results in bacterial peritonitis.
euphoria; reversal of Normal EEG. ○ Septicemia may result.
day-night sleep patterns ○ Adult respiratory distress syndrome and
acute renal failure are possible
complications.
2 Increased drowsiness; sterixis;
A fetor ● Causes
disorientation; hepaticus. Abnormal ○ Gallstones
inappropriate behavior; EEG with generalized ○ Alcohol abuse
mood swings; agitation slowing of the cerebral ○ Sudden onset, may follow intake of large
function. meal or large amount of alcohol
● Manifestations:
3 tuporous; difficult to
S sterixis;
A increased ○ Abdominal pain (constant mid epigastric,
rouse; sleeps most of deep tendon reflexes; periumbilical that may radiate to back or
time;markedconfusion; rigidity of extremities. flank and substernal with DOB aggravated
incoherent speech EEG markedly by eating)
abnormal. ○ Client assumes fetal position to relieve
pressure (celiac plexus nerve)
9
○ Involuntary abdominal guarding ○ Nonpharmacologic:
○ Decreased or absent bowel sound ■ Position (Knee chest, fetal) - to
○ Turner's sign - bluish discoloration of the decrease pain and provide amore
flank (ecchymoses) relaxed method in handling pain
○ Cullen's sign - periumbilical bluish and colic
discoloration ■ Relaxation techniques, restful
● Signs of shock environment
○ Caused by hypovolemia
○ Diet High protein, CHO; low fat
● Low-grade fever until infection develops ○ Small frequent feeding
○ Body temperature may then rise significantly. ○ Avoid caffeine, alcohol
● Abdominal distention and decreased bowel sounds ○ WOF signs of complications:
○ Decreased peristalsis and paralytic ileus ■ Nausea and Vomiting,
● Diagnostic tests: ■ Abdominal distension,
○ Serum amylase levels - first rise, then fall ■ Persistent weight loss,
after 48 hours ■ Severe epigastric pain or back pain,
○ Serum lipid levels are elevated. ■ Irritability,
○ Hypocalcemia ■ Confusion,
■ Intheelectrolytes,calciumbindsto ■ Fever
the necrotic areas in the pancreas
○ Leukocytosis E. COMPLICATIONS OF DIABETES
● Treatment
● ne of the most common disease worldwide
O
○ Oral intake is stopped. ● By population 60-70% have diabetes
○ Treatment of shock and electrolyte ● Ranges from Type 1, Type 2, and Gestational
imbalances ● Complications have 4 groups:
○ Analgesics for pain relief ○ Hypoglycemia
● Autodigestionisakeyfactor,whereinthedisease ○ Hyperglycemia
process takes place ○ DKA
○ HHNKS - Hyperosmolar Hyperglcemic
Nonketotic Syndrome
● Type2DM-youhaveinsulin,butcannotcoverforthe
increasing sugar leading to hyperglycemia. Lacking
insulin, the insulin receptors cannot be opened for
sugar to enter the cell so sugar stays in the blood
causing viscosity. The osmotic and oncotic pressure
areindisequilibrium.Thevolumethatarefilteredare
unequal. In the kidneys, the GFR malfunctions. The
volume increases leading to polyuria, resulting to
cellular dehydration. Negative feedback mechanism
lead to signal thirst resulting to polydypsia. Lacking
metabolic outcome, sends signal to acquire more
energy through form of food leading to polyphagia.
○ After perfusion is not enough, the delay in
perfusion and increase in volume and
electrolyte imbalances, the large vessel is
● Medical Management effected. 1. in the heart there is increased
○ Drug deposits of plaque leading to CAD, 2.
■ Analgesics (Demerol) delayed perfusion in brain leads to
● Your morphine can cause development of stroke
probleminthesphincterof ○ HgbA1c - affinity binding to hemoglobin,
oddi, DOC is Demerol definitive diagnosis
■ Smooth muscle relaxants ○ Prone to infection 1. UTI 2. Pulmonary
(papaverine,nitroglycerine)-relieve infection due to sugar
pain ○ Diabetic diet - carbs proteins andfatshave
■ Anticholinergic (atropine) - certain percentage
decrease pancreatic stimulation ■ Carbs 45-65%, Protein 15-25%,
■ Antacids decrease pancreatic Fats 20-35%
stimulation ○ Renal diet - control electrolytes
■ H2 antagonists, vasodilators ○ Manifestation of hypoglycemia can mimic
○ Diet modification stroke that is why we need to check
■ NPO neurological signs and deficits
■ Peritoneal lavage ○ Type 2 DM is from lifestyle, and family
● Nursing considerations
○ Administer analgesics, and other meds HYPERGLYCEMIA
○ Do not give Morphine
● igh glucose
H
■ Causes spasm in the sphincter of ● The sugar is not used by the cells, not metabolized
oddi ● Question what happens to liver, insulin, and pancreas
○ Withhold food/fluid to decrease pancreatic
stimulation in acute case (NPO) Somogyi phenomenon
○ NGT
10
● ypoglycemia usually at night followed by
H
compensatory rebound hyperglycemia (lasts 12 to
72hours).Usuallycausedbytoomuchinsulinoran
increaseininsulinsensitivity.Canbestabilizedby
gradual lowering of insulin dose and increase in
diet at the time of the hypoglycemic reaction.
● When there is insulin sensitivity, the sugar does not
go into the cells
● Insulin serves as key by which it opens the insulin
portals so that the sugar can enter the cells for
metabolism
● Mababa sugar tapos bigla tataas
● Hypoglycemia at night followed by rebound
hyperglycemia in the morning.
● Hypoglycemia triggers the release of ● loodsugarforsomogyieffect,thereishypoglycemia
B
counter-regulatory hormones: and at the peak there will be insulin sensitivtiy
○ epinephrine, glucagon, GH, cortisol, all of therefore rebound hyperglycemia (SO MUCH
which promote hepatic glucose production INSULIN,thereisinsulinsensitivitythatiswhysugar
and also induce transient insulin resistance increases)
● Treatment consistsofdecreasinginsulinrequirement ● Indawnphenomenon,fromepisodeofhypoglycemia
or changing time of administration to hyperglycemia, it is continuous as morning
approaches (DOWN, there islittleinsulinthatiswhy
Dawn phenomenon there is hypergylcemia)
● Both maybe managed by adjusting meals during
● loodSugarisnormaluntil3amthenbeginstorise
B mealtimes:
inearlymorninghours.Glucosereleasedfromliver ○ Somogyi - take dinner early
in early A.M. needs to be controlled. Altering time ○ Dawn - have bedtime snack
anddoseofinsulin(NPHorultralente)bytwoortwo
units stabilizes the pt.
● Early morning rise in blood glucose with no
hypoglycemia during the night.
● Appears to be the effect of growth hormone:
○ increased liver glucose production
○ decreased peripheral tissue use
○ increased clearance of insulin from plasma
may be a factor.
oth are hyperglycemic condition that occurs in the
B
morningbut with different mechanism ● eaktime-thebodysitillconsumessugarbecauseof
P
metabolic processes
Somogyi effect Dawn phenomenon
HYPOGLYCEMIA
an made. Due to poor P
M hysiological secretion of
● ow or decreased sugar
L
diabetes management. hormones (growthhormone, ● Occurs as a result of an imbalance in food, activity,
cortisol, cathecolamines) and insulin/oral antidiabetic agent
Thosewithtype2DM,thisis ● Signs and symptoms
the effect Physiologic reaction to high ○ ADRENERGIC SIGNS (early s/sx)
level of stress esp. during ■ Sweating,coldclammyskin,tremor,
release of cortisol pallor, tachycardia, palpitations,
nervousness from the release of
In the night, patient In the night, the insulin adrenalinewhenbloodglucosefalls
becomes hypoglycemic actions will eventually rapidly
due to the sensitivity and wear off and at the same ■ The body will make a way to
action of the insulin and time counter-regulatory provide for the decrease in sugar
the drugs -> glucagon is hormones are secreted -> ■ No management and progresses,
released -> glycolysis -> hyperglycemia because late stage happens
hyperglycemia there is little amount of ○ NEUROLOGIC (late s/sx)
circulating insulin ■ Light-headedness, headache,
ensitivitytoinsulinleadsto
S confusion, irritability, slurred
sugar not reacting, sugar A s morning approach, the speech, lack of coordination,
doesnotenterthecells,and sugar of pt increases stagerring gait
stays in blood and outside
● Sugar is food, fuel for body processes
the cells ● Sugar must be metabolized
● If gone, there is no input for cells to metabolize
● Sugar is energy, there is body weakness without it
● For sugar to enter the cells, it needs the key to
penetrate cells - through insulin.
11
● ithout insulin,glucoseremainsinthebloodleading
W ● Precipitating events:
to hyperglycemia ○ DKA - No insulin, addedphysiologicstress,
● Ifthereistoohighinsulinlevelbecauseofdiff.factors infection, sepsis, stroke, MI
(stress/hormones), sugar is metabolized quickly ○ HHNKS - Physiologic distress
● Commonlyabusedtermwhenhungryis“naghypo”- ● Which between the two is lifestyle related?
ifthisistheproblem,givesugar(whateverislost,you ○ Both can be categorized however since
give) HHNKSisabsolutelyrelatedtotype2DM,it
● A diabetic patient have at least 6 small meals a day. is more affinitive to lifestyle diabetes
○ Breakfast - moderate amount
○ Snack - biscuits
○ Lunch - small to normal portion CHARACTER DKA HHNKS
○ Snack in the afternoon - biscuit, banana, -ISTICS
kamote, oatmeal
○ Dinner atients
P most C
an occurintype an occurintype
C
○ Before sleep, there is a option for snack commonly 1 or type 2 1 or type 2
○ Givesnackstosustainsugarandavoidhypo affected diabetes; more patients; more
and hyperglycemia common in type common in type
1 2 diabetes,
especially elderly
patients with type
2 diabetes
recipitating
P mission
O of P
hysiologicstress
event insulin; (infection,surgery,
physiologic stress CVA, MI)
(infection,surgery,
CVA, MI)
Onset Rapid (<24 hrs) Slower (over
everal days)
s
lood
B glucose U
sually >250 U sually >600
levels mg/dL (>13.9 mg/dL (>33.3
mmol/L) mmol/L)
Arterial pH level <7.3 Normal
● heck CBG to determine hypoglycemia
C
● TREATMENT erum andurine Present
S Absent
○ 15-20 G fast acting carbohydrates ketones
■ Half-cup (4oz) juice, 1 cup skim
milk, 3 glucose tablets, four sugar Serum osmolality 300-350 mOsm/L >350 mOsm/L
cubes, five to six pieces of hard
candy may be taken orally. lasma
P <15 mEq/L Normal
○ Supplies glucose from sucrose, starch, and bicarbonate level
protein sources with some fat to delay
gastric emptying and prolong effect
UN
B and Elevated Elevated
● SIMPLE CARBOHYDRATE TO TREAT
creatinine levels
HYPOGLYCEMIA
○ *3 or 4 commercially prepared glucose
tablets Mortality rate <5% 10% - 40%
■ CHILD: 2-3 glucose tabs
○ *4-6 ounces of fruit juice or regular soda DIABETIC KETOACIDOSIS (DKA)
■ CHILD: 1⁄2 cupor120mloforange ● cutecomplicationofdiabetesmellituscharacterized
A
juice or sugar-sweetened juice by hyperglycemia, ketonuria, acidosis and
○ *6-10 Life Savers or hard candy dehydration
■ CHILD:3-4hardcandiesor1candy ● PATHOPHYSIOLOGY AND ETIOLOGY
bar/chocolate ○ Insulin deficiency prevents glucose from
○ *2-3 teaspoons of sugar or honey being used for energy, forcing the body to
■ CHILD: 1 small box of raisins metabolize fat for fuel.
● BOARD QUESTION: Patient has slurred speech, ○ Free fatty acids, released from the
leaningtowardsneuromanifestationwhatdoyougive metabolism of fat, are converted to ketone
forhypoglycemia-GivebolusD50ifinhospital,ifnot bodies in the liver.
in hospital activate health and bring to ER ○ Ketone bodies results metabolic acidosis
● Nosugar,noenergy.Thecellswilllookforsomething
COMPARISON OF DIABETIC KETOACIDOSIS (DKA) AND to metabolize
HYPEROSMOLAR NONKETOTIC SYNDROME (HHNKS)
● Sugar needs insulin to enter the cells
● Pathogenesis: ● No insulin, suagr stays in blood
○ DKA - Type 1 (No Insulin) ● Metabolism isconstant.Sincethebodydoesn’thave
○ HHNKS - Type 2 insulin or missed doses of insulin, and metabolism
12
ontinues, sugar does not enter the cells therefore
c
celss cannot metabolize sugar therefore no energy
● Cells as compensatory mechanism will find fats for
energy, fats as fuel
● Cellwillmetabolizefats,andendproductisACIDS,
FATTY ACIDS, OR KETONES
● Ifketonescontinuetodevelopinthebody,itisin
danger of metabolic acidosis
HYPEROSMOLAR NONKETOTIC SYNDROME (HHNKS)
● Pathogenesis: Type 2 DM
● You have insulin, however there is low level in the
body, so there is sugar going to the cell(BUTLOW
LEVELS)
● NO KETONE FORMATION BECAUSE OF THE
PRESENCE OF INSULIN
● Is an acute complication of diabetes mellitus
characterized by hyperglycemia, dehydration and
● Increased K for mild cases and decreased K for
hyperosmolarity
severe cases - one of the characteristics of DKA is
● Pathophysiology and Etiology
polyuria. every time they urinate a portion of
○ Prolonged hyperglycemia with glucosuria
electrolytesgoesoutofthebodyleadingtoelectrolyte
produces osmotic diuresis
imbalance and even dehydration
○ Lossofwater,sodiumandpotassiumresults
● If sugar exceed more than 300mg/dl the danger is
in severe dehydration causing hypovolemia
COMA
○ Hyperosmolarity results from excessive
● Signs and symptoms
blood sugar and increasing sodium
○ Early
concentration in dehydration
■ Polydipsia, polyuria
○ Prolonged hyperglyciemia and low level of
■ Fatigue, malaise, drowsiness
insulin, so sugar can penetrate cell but not
■ Anorexia, N/V
all because of low level of insulin
■ Abdominal pain, muscle cramps
○ Still have polyuria, polydypsia, and
○ Later
polyphagia therefore there is loss of water
■ Kussmaul respiration (deep
and electrolytes and still there is
respirations)
hyperosmolarity
■ Fruity, sweet breath
○ ABSENCE OF KETONES
■ Hypotension, weak pulse
○ Insulin continues to be produced at a level
■ Stupor, coma
that prevents ketosis
● Diagnostic Evaluation
○ Increased blood viscosity decreases blood
○ Serumglucoselevelisusuallyelevatedover
flow to the organs
300mg/dl
○ Intracellular shifting produce neurologic s/sx
○ Presence of ketone bodies
○ Serum bicarbonate and ph are decreased
○ Low Na and K
○ Elevated BUN, Creatinine and hematocrit
○ Urine gravity and concentration increased
● Management
○ I.V Fluids to replace losses from osmotic
diuresis, vomiting
○ I.V insulin drip
○ Electrolyte replacement
● BOARD/NCLEX QUESTION: What is compatible
insulin for IV route? Regular insulin
● Guidelines for Safe Practice:
● Signs and Symptoms
○ Early
13
■ olyuria, dehydration,
P fatigue, GLUCAGON
malaise, N/V
● rom the pancreas
F
○ Late ● Hormone secreted by the alpha cells oftheisletsof
■ Hypothermia, seizures, stupor, Langerhans in the pancreas
● Diagnostic Evaluation ● Increase bloodglucosebystimulatingglycogenolysis
○ Serum glucose and osmolality are greatly in the liver
elevated
● given SC, IM or IV routes
○ Serumsodiumandpotassiumlevelsmaybe ● Used to treat insulin-induced hypoglycemia when
elevated (at the beginning) semiconscious/unconscious
○ BUNandcreatininemaybeelevateddueto
dehydration
○ Urine specific gravity is elevated
● Management
○ Treat dehydration - Correct fluid and
electrolyte imbalances with I.V fluids
■ If potassium is down, can have
cardio problems
■ If sodium is down,canhaveneuro
problems - SEIZURE
○ Provide insulin via I.V drip to lower plasma
glucose
○ Evaluate complications, such as stupor,
seizures, or shock, and treat appropriately.
○ Identify and treat underlying illness
ORAL HYPOGLYCEMIC AGENTS
● Sulfonylureas
○ Chlorpropamide (Diabinase)
○ Tolbutamide (Orinase) F. MACRO AND MICROVASCULAR COMPLICATIONS OF
○ Glimepinide (Solosa) DIABETES
○ Acetohexamide (Dymelor) ● Chronic complications
● Prandial Glucose Regulator ● Too much sweetness cankill.Avoidbeingtoosweet
○ Repaglinide (Novonorm) because it will kill you
○ Rosiglitazone (Avandia) ● It will kill you gently, softly, but surely
● Non-sulfonylureas ● Macroangiopathy (Macrovascular) - large system
○ Metphormine (Glucophage) involvement / large vessels
○ Precose (Acarbose) ○ CVA / Stroke
○ Rosiglitazone (Avandia) ○ CAD
○ PVD
INSULIN ○ Also kidney failure
● ey for sugar to be metabolized
K ● Microangiopathy (Microvascular) - minute vessels
● Without insulin, the sugar will just float in the blood involved
leading to hyperglycemia ○ Retinopathy
● Insulin increases glucose transport into cells & ○ Nephropathy
promotes conversion of glucose to glycogen, ○ Neuropathy
decreasing serum glucose levels
● Primarily acts in the liver, muscle, adiposetissueby
attaching to receptors on cellular membranes &
facilitating transport of glucose, potassium &
magnesium
● eet - in terms of pressure gradient there is higher
F
pressureinupperthanlower,givingslowerperfusion
● In between meals, can give intermediate acting insulin
in the feet compared to upper portion. Can end in
● In Diabetes, need INSULIN, DIET, and EXERCISE
amputation
○ In pre-dm - need change lifestyle already
MACROANGIOPATHY
14
CVA ● haracterized by distal symmetrical polyneuropathy
C
involving the lower extremities
● haracterized by hypertension, increase lipids,
C ● ASSESSMENT
smoking, and uncontrolled blood glucose ○ Decrease sensation
● ASSESSMENT ○ Diminished ankle jerk response
○ Increase BP ● When there is wound on the foot, there is delayed
○ Change in mental status wound healing
○ Hemiparesis ● The person cannot identify any form of pain on the
○ Aphasia foot
● If you have DM and did not change your lifestyle, ● Mayleadtoinfection,removedigitperdigit(proneto
BUY 1 GET5:Stroke,Heartfailure,End-stagerenal infection)
failure, PVD, Foot problems ● Ascending infection-sugaristheculpritforbacterial
growth
CAD
Autonomic Neuropathy
● haracterized by ATHEROSCLEROSIS
C
● ASSESSMENT
● haracterized by impotence and sexual dysfunction
C
○ Asymptomatic ● ASSESSMENT
○ Symptoms of angina leading to MI ○ Changes in erectile ability, ejaculation and
libido
PVD ○ Erectile dysfunction, absence of early
morning erection
● haracterized by absenceofpedalpulsesleadingto
C ○ Decrease vaginal lubrication and
ischemic gangrenous tissues dyspareunia
● ASSESSMENT
○ Symptoms of PAOD (peripheral arterial G. RENAL FAILURE
obstructive disorder) and Vascular Disorders
Acute Renal Failure
MICROANGIOPATHY
● udden decline in renal function, usually associated
S
Retinopathy with increase in BUN, creatinine & electrolytes
● Categories:
● here will come a point of blindness if DM is NOT
T ○ Pre, Intra and Post-renal
MANAGED ● Reversible
● Characterized by appearance of hard exudates,blot
hemorrhages and microaneurysms of the retina Acute Renal Failure: Pre-renal
● Culprit is sugar, hyperglycemia. Slower circulation
because blood is viscous, perfusion is not good ● Decreased renal tissueperfusionfrom:
● ASSESSMENT ○ Hypovolemia
○ Asymptomatic in early stages ○ Shock
○ Acute visual problems ○ Hemorrhage
■ Floaters, flashing of lights, blurring ○ Burns
of vision, may indicate retinal ○ Impaired cardiac output
detachment ○ Diuretic therapy
● There is notenoughperfusioninthekidneythatcan
Nephropathy cause injury to the kidenys and malfunction
● haracterized by thickening of the glomerular
C Acute Renal Failure: Intra-renal
basement membrane and renal vessel sclerosis
leading to diminishing renal function
● emember:Parenchymal.
R
● Kidneyscanshrinkleadingtooliguriaandebenliedto ● We look into the disease at the parenchymal or
Kidney Injury / Kidney Failure cellular level
● GFRisthecapabilityofthekidneytofiltereverything ● AGN - acute glomerulonephritis
in and out of the body. ○ Infection of kidney due to immune response
● GFRisdestroyed.Bloodisviscous,hardforkidneyto ○ Previous infection from group A beta
function hemolytic streptococcus
● ThereisincreasedGFR,thedangerisnoteverything ○ S/SX:proteinuria,hematuria,oliguria,edema
isfilterdthatiswhysugar,albuminescapesandgoes and HPN
to the urine ○ The cells are attacked by different
● Leadstosedimentsintheurine:protein,blood,sugar, microorganism that impairs the kidney in
albumin terms of its functioning
● ASSESSMENT ● CGN - chronic glomerulonephritis
○ Increased GFR ○ Non-infectious, slowly developing disease
○ Microalbuminuria ○ S/SX: same with AGN
○ Elevated BUN, CREA ● Nephrotic Syndrome
○ Gross Proteinuria ○ Severely damaged glomerular activity that
leads to increased capillary permeability
Peripheral Neuropathy
15
S/SX: proteinuria, hypoalbuminemia, and
○ ■ rom the moment kidney is
F
yperlipidemia
h reperfuse
○ Caused by CGN, DM, and SLE ■ Damaged nephrons recover
● cute Tubular Necrosis
A ■ Initiationphasewillseteverything,if
thelifestyleisnotgood,thereistoo
Acute Renal Failure: Post-renal muchsalt,toomuchdamagetothe
kidney then the oliguric-anuric
● ue to obstruction or disruption to urine flow
D phase will continue
anywhere along the urinary tract: ■ Chances of going into diuretic
○ Trauma phase depends on the
○ Urethritis oliguric-anuric phase
○ Pyelonephritis ○ Due to partially regenerated tubes/recovery
○ Urolithiasis of damage
○ Injuries to the bladder and urethra ○ Hypovolemia / hypotension
○ Cancer of the bladder ■ From production of urine volume
○ Blood clots ○ Tachycardia
○ BPH - (Benign Prostatic ■ Compensatory mechanism
Hyperplasia/Hypertrophy) ○ Level of consciousness improves
■ Fluids and electrolytes start to get
Acute Renal Failure: Clinical Course normal
■ Toxins are removed on the system
● INITIATION ● RECOVERY PERIOD
○ Exposed to causes wheter it is pre-renal, ○ Expect urine volume returns to normal
intra-renal, or post-renal ○ May take 3 months to 1-2 years from the
○ Exposed to different factors that can initial onset
start/expose the kidney to have injury ■ Dependent on oliguric-anuric and
○ Maytakesometimebecausethekidneyare diuretic phase
compensating ○ Urine volume is normal
○ Glomerualfiltrationrateisdamagedandthe ○ Increase in strength occurs
ability of function is damaged as well ○ BUN stable and normal
● OLIGURIC-ANURIC PHASE ■ Along with fluids and electrolytes
○ From oliguria to anuria parameters
○ Decres in urine over 24 hours
○ Set the course as it progresses Acute Renal Failure: Management
○ <400ml/24 hr.
○ May last 8-15 days ● Monitor I&O
○ Hyper K, Mg, Phosphate, Hypo Ca, ○ Kidneyseliminatewaste,andreabsorbwhat
Metabolic acidosis needs to be reabsorbed
○ The longer the duration the less chance ○ Need parameters to measure fluids
of recovery ● Weighing
○ Decreased Sp gravity ○ Indicator of fluid and electrolyte management
■ Because of the loss of electrolytes
● Infection monitoring
○ Anorexia, N/V ● Examine gross and occult blood
■ May develop weight loss ● Diet
○ HPN ○ Convalescence(CHONmoderate,increase
○ Decreased skin turgor CHO)
■ From fluid and electrolyte ○ Restrict protein intake (Oliguric)
imbalances ■ Also anything that can prolong the
○ Pruritus oliguric-anuric phase
■ Resultoftoxindepositsthatarenot
● Electrolyte management
filtered by the kidneys ● Neurologic assessment
○ Tingling of the extremities
■ From hypocalcemia Acute Renal Failure: Nursing Interventions
○ Drowsiness-Disorientation-Coma
○ Edema
● onitor fluid and electrolytes
M
○ Dysrrythmias ● Baseline appearance and amount of urine
○ Signs of congestion (CHF), pulmonary ○ Document color of urine, and volume
edema
● Monitor I and O
○ Signs of pericarditis ● Administer IVF as ordered
○ Signs of Acidosis ● Weigh daily
● DIURETIC PHASE ● Monitor lab results
○ Insituationwherethereisacutekidneyinjury ● Monitor V/S: HPN
and treatments are successful and the pt ● Promote optimal nutrition
kidneyswereabletoadapttothetreatment, ● TPN/enteral feeding
the oliguric-anuric phase becomes shorter ○ If unable to take food orally
and then sucessfully goes into the diuretic ● Provide care for pts receiving dialysis
phase
○ Urine output in 2-3 wks: (4-5L/day) Chronic Renal Failure
16
● rogressiveirreversibledeteriorationofrenalfunction
P
whichend fatally in uremia
● ecreased renal function
D
● Dialysis or kidney transplant is necessary ● No accumulation of metabolic waste products
● Predisposing factors: ● Kidney compensates
○ May follow ARF ● Nocturia and polyuria
○ Recurrent infections ○ At rest, kidneys are reperfused by
○ Exacerbation of nephritis oxygenated blood
○ Urinary tract obstruction ○ At the peak of the moment kidney are
○ DM reperfused, that’s the time kidney functions
○ HPN that’s why there is nocturia
○ Renal artery occlusion
○ Autoimmune disorders Chronic Renal Failure: Stage 2 (Renal Insufficiency)
● On ARF do pt receive dialysis? YES
● One of the indications for dialysis is when the
● ccumulation of metabolic wastes
A
potassium level is high. It is detrimental to cardiac ● Oliguria (gets worse)
function ● Edema
● Also cardiac overload, manifesting signs of edema, ● Decreased responsiveness to diuretics
difficulty of breathing, and the pt is not urinating,
dialysis is indicated Chronic Renal Failure: Stage 3 (End Stage)
○ Also level of BUN and Creatinine
● What access is used? Emergency intra-jugular
● xcessive metabolic waste accumulation
E
catheteraccessorfemoralcatheterdependingonthe ● Unable to maintain homeostasis
condition ● Dialysis/transplant
○ IfexperiencingCOPDoraggravatedCOPD, ● Kidneys severely damaged
most likely the ptwillhavebarrelchestand ● Constant dialysis is needed, andideallyatransplant
the lungs may be punctured, uses fem cath too
○ But watch out for infection because of its
proximity to the reproductive organ Chronic Renal Failure: Signs and Symptoms
○ Most accessible is IJ cath
● #1 CAUSE is ARF. If exposed to ARF or have a ● ocusonthesecuritybecausemanifestationtendsto
F
history, you are not safe from CRF get worse as well
● Takecareofyourkidneysbecauseyoudon'twantto ● NaandWaterretention-incBV-edema-HPN-CHF
get CRF becauseit is irreversible - ascites
● Lifetime dependent on dialysis ifkidneytransplantis ● Decreased Renal tissue perfusion - Dec urine
not available formation - Renin activation - Angiotensin and
● HISTORY OF ARF IS #1PREDISPOSINGFACTOR aldosterone production - Inc BV - Inc BP
FOR CRF ○ RAAS activated at an exaggerated level
● Decreased H ion excretion - Metabolic acidosis,
Chronic Renal Failure: Diagnosis Kussmaul's respiration
○ If experiencing diabetes, expect that
● lot of parameters will tell you something is wrong
A metabolic acidosis may happen
● Serum crea - elevated (normal 0.5-1.5 mg/dl) ● Decreased nitrogenous excretion - Azotemia - Toxic
● Serum BUN - elevated (normal 20-30 mg/dl) to CNS leading to dec LOC, Convulsions, Coma
● Serum electrolytes - all electrolytes are elevated
● Decreased secretion of erythropoietin - Anemia
except for HCO3 and Calcium ● Decreased electrolyte excretion - Elevation of
● CBC - anemia (due to reduced erythropoietin electrolytes in the blood
production)
● Formation of active vit D - Hypocalcemia
○ Check level of RBC ● Muscle twitching and numbness of extremities
● Renal Ultrasonography - to estimate renal size and ● Fluid overload
obstruction ○ Why experiencing DOB
○ Decreased size and obstruction ● Uremic Frost: urea crystals from perspiration (face,
● Other tests that may help in detecting the cause eyebrows, axilla, groin)
● Low albumin - check if have edema
Chronic Renal Failure: Clinical Course ● Hypocalcemia - check the nerves
● Check the electrolyte content of the food
● here is staging, but look into GFR
T ○ e.g. You can’t give whole banana since it’s
● Functional gromeulurus decreases full of potassium
● Decreased renal reserve: 40-70 GFR
● Renal insufficiency: 20-40 GFR Chronic Renal Failure: Management
● Renal failure: 10-20 GFR
● End-Stage Renal Disease: ↓10 GFR
● estrict water and sodium intake
R
● Bothkidneysareseverelyaffectedandrenalfunction ● ABG monitoring and NaHCO3 administration
is absent ○ To check if experiencing metabolic acidosis
● Talking about damage on BOTH kidneys and respiratory distress
● Expectrenalfunctionisabsentandmanifestationswill
● Neurologic assessment
occur ● Dialysis
● Diet (CHON restriction, inc CHO)
hronic Renal Failure: Stage 1 (Diminished Renal
C ● Give vit D and calcium supplement
Reserve) ● Give synthetic erythropoietin (epogen)
17
● anage electrolyte imbalance
M
○ eigh
W
● Anti HPN ○ V/S q 30
● Aluminum Hydroxide gel ○ Withhold all anti HPN, sedatives unless
○ For pruritus ordered otherwise
● Don’t give antihpn and antibiotics during dialysis ■ May causesuddendecreaseinBP
○ antiHTN - the blood pressure will go down during dialysis
further ○ (Monitor for bleeding heparinized blood)
○ antibiotics - the medication will be dialyzed ○ Monitor laboratory values
● IJcathisusedaslastoptionorforemergencyaccess ● Post-nursing care
or only to draw blood for lab tests ○ Weigh
○ WOF Hypovolemic shock
Chronic Renal Failure: Nursing Interventions ● Disequilibrium Syndrome
○ Mabilis ang hatak
● onitor V/S
M ○ Rapidremovalofsolutesfromthebloodthan
● Monitor I and O from the brain
● Monitor Wt: ½ - 1 lb increase means fluid retention ○ Monitor the signs
● Monitor BUN, Crea, electrolytes ■ N/V, Anorexia,IncBP,Paresthesia,
● Monitor blood pH - Administer NaHCO3 Headache, Confusion, Seizures
● Monitor LOC ○ Inform MD
● Assess for dysrhythmias (hyperK) - ECG ○ Shorter period of dialysis and at reduced
● Monitor for fluid overload/congestion blood flow rate
● Restrict Na ■ Slow dialysis / SLED - conducted
● Fluid limits (400-1000 ml/day) over 6hourperiodovertheregular
● Administer Sodium polysterene sulfonate(kyexelate) dialysis which is 3-4 hours
to decrease K
● Avoid nephrotoxic drugs Dialysis: Peritoneal Dialysis
● Provide for care on patients receiving dialysis
● ses special catheter, Tenkoff catheter in the
U
Chronic Renal Failure: Specific Interventions peritoneum to allow exchange to happen
● Nursing care
● ssess for signs of uremia (fatigue,lossofappetite,
A ○ Weigh
decreased urine output, apathy, confusion, High BP, ○ Void
edema of face and feet,itchyskin,restlessnessand ○ Warm dialysate to pt's body temp
seizures) ○ Assist in trocar insertion
● Signs of Hyperphosphatemia (paresthesias, muscle ○ Inflow: allow 1-2 L dialysate to flow
cramps, seizures, abnormal reflexes) unrestricted (10-20 mins)
○ Give amphogel administration ■ Putting dialysate within in the
● Promote GI functioning (n/v, stomatitis, anorexia, peritoneum
bleeds) ○ Dwell: allow dialysate to stay in the
● Promote skin integrity peritonium (30-45mins)
● Monitor for bleeding (avoid IM injections) ■ The fluid will now attract all the
metabolic waste so that when it’s
Dialysis drained all waste products are
drained as well
● ost significant management of kidney failure
M ○ Drain: unclamp and drain by gravity
● PURPOSES ■ After it is drained, there should be
○ Want to have kidney function andcorrecta increased volume
lot of parameters ■ Di maganda if nag retention
○ Dialysis is the mechanical kidney ● Nursing Interventions during treatment
○ Remove the product of protein metabolism ○ Monitor signs of infection
○ Maintain safe levels of e+ ○ Monitor V/S
○ Correct acidosis and replenish HCO3 ○ Monitor resp distress, pulmonary edema
○ Remove excess fluid ○ Monitor HPN, Hypotension
● Types ○ Monitor catheter site for bleeding
○ Peritoneal Dialysis ○ Nausea and vomiting during dialysis
○ Hemodialysis ○ Do notallowprolongeddwelltimeasitmay
cause hyperglycemia
Dialysis: Hemodialysis ○ Turn side to side to aid outflow
○ Monitor color and amount of dialysate
● Nursing Interventions on AV fistula formation ○ Monitor I and O
○ Do not use arm with AV fistula for ○ Observe dialysate
venipuncture, BP taking, IV, and injections, ■ Clear, pale yellow- Normal
and lab extractions ■ Cloudy- Infection, peritonitis
○ Check patency of fistula ■ Brownish- perforated bowel
○ Check for bleeding ■ Bloody - common in first few
○ Check pulses for patients with subclavian exchanges but abnormal if it
and femoral cannulation persists
● ALWAYS CHECK FOR THE BRUIT ○ Protein loss
● Pre-nursing care ● CAPD(Continuous Ambulatory Peritoneal Dialysis)
18
○ one at comfort of pt’s home
D ● GIB typicallypresentsashematemesis(vomitingof
U
○ You teach the pttodoperitonealdialysisat bloodorcoffee-groundappearingmaterial)ormelena
home (black, tarry stools)
Kidney Transplant Causes
● Donor and Recipient Preparation
● an be caused by variety conditions
C
○ Donor ● OvertGIbleedingwithhematememsisandmelenaor
■ Living and Cadaveric (k akaharvest hematochezia
lang) ● Also with non-specific symptoms r/t iron deficiency
○ Recipient preparation anemia
■ Drugs:
● Classified to Upper and Lower GI bledding
→ Immunosuppresive and ● Upper GI bleeding accounts for 70-80% of all GI
Antibiotics prophylactically hemorrhage
■ Note for Rejection (dec urinary ○ Source ofbleedingisproximaltoligament
output,fever,pain,tendernessover of thrice
site, edema, HPN, wt gain, rise in ● Lower GI bleeding account for 20-30% of GI
creatinine) hemorrhages
→ This is a complication ○ Source isdistal ligament of thrice
→ WOF decreased kidney ● Occult blood GI bleeding is bleeding in quantitiies
function AFTER the toosmalltobemicroscopicallyobservablethat’swhy
transplant they request occult blood test
→ Kidney is not adjusting to ● Overt GI bleeding can me macroscopically
the system obeserved and seen withaccompanyings/ssuchas
■ Rejection and Infection anemia and tachycardia
■ Isolation (Reverse) ● Obscure GI bleeding that persist or reccurs after
■ Also counselling, ethicolegal initial negative evaluation
counselling ● Major causes include gastric or duodenal ulcer,
■ Prepare body, there should be no severe or erosive gastritis/duodenitis/esophagitis,
infection esophagogastric varices, portal hypertensive
● Assessment for rejection gastropathy, angiodysplasia, arteriovenous
○ Fever malformation, Mallory-Weiss (esophageal tear), and
○ Malaise upper GI polyps/cancers. The source of bleeding
○ Increased WBC cannot be determined in 10-15% of patients with
○ Graft tenderness UGIB.
○ Deteriorating renal function ○ Errosive / Inflammatory
○ Acute HPN ■ Upper GI - peptic ulcer disease,
○ Anemia esophagitis, errosive gastritis or
○ We expect the urine will become normal, duodenitis
however if the kidneys fail, there is rejection → PUD - break in the
● Rejection mucosal lining of the
○ Hyperacute stomach
■ Immediately within 48 hrs ■ LowerGI-causedbydiverticulosis,
■ Int: Remove Rejected kidney inflammatory bowel disease,
immediately Crohn’s disease, inflammatory
○ Acute: 6 wks - 2 yrs diarrhea, multitidue of bacterial
■ Reversible infection
■ High dose steroids (for → Diverticulitis - multiple
immunosupression) outpouching that weakens
■ Watch closely for kidney function the wall
because rejection may occur ○ Vascular
○ Chronic ■ Upper GI - esophageal varrices,
■ Months to years gastric ectasia, lesions
■ Irreversible → Esophageal varrices -
■ Mimics CRF dilates mucosal veins that
● If pt get kidney and it is successful,functionwillget causes bleeding. S/t to
better, but it depends on their lifestyle portal hypertension
● There will always be RISK → Gastricectasia-dilationof
● Make sure you are compliant small blood vessels w/in
the stomach
H. GASTROINTESTINAL BLEEDING ■ Lower GI - hemorrhoids, ischemia,
AV malformation
Management of Upper GI Bleeding → Hemmorhoid - can be s/t
to abnormal enlargement
● In the U.S., acute upper gastrointestinal bleeding or protrusion causing
(UGIB) is more common than lower gastrointestinal bleeding
bleeding (LGIB). → Ischemia - due to colitis
○ Tumor
19
■ pper GI - Esophageal tumor,
U nd
a may require
colorectal cancer or anal cancer, transfusion of freshfrozen
colonic polyps, trauma, hyatal plasma (FFP) orplatelets.
hernia, Mallory Wise syndrome, Also consider patient use
Brow hand syndrome of anticoagulants or
■ Lower GI bleeding - lower antiplatelet agents.
abdominal trauma, anorectal → Dementia or hepatic
trauma, portal hypertensive encephalopathy could
gastropathy, coagulopathy, anal cause aspiration of GI
fissures contents; endotracheal
intubation may be
● a
c pid assessment and management of airway, considered in these
breathingandcirculationistheinitialpriority.Oncethe patients.
patientisstabilized,thegoalistoassesstheseverity ○ Medication History
of the bleed, identify the potential source, and ■ Aspirin and non-steroidal
determine ifthereareunderlyingconditionsthatmay anti-inflammatorydrugs(NSAIDs)
affect the management. (may cause peptic ulcers)
○ History → Side effect will cause
■ Previous episodes of upper GI peptic ulcers
bleeding; approximately 60% of ■ Antiplatelet agents and
patientswithhistoryofGIbleedare anticoagulants (may contribute to
bleeding from the same lesion. GI bleeding)
■ Liver disease or alcohol abuse ■ Use of corticosteroids can cause
(may cause varices or portal peptic ulcer disease
hypertensive gastropathy) ■ Serotonin reuptake inhibitors
■ Abdominal aortic aneurysm or (SSRI), calcium channel
aortic graft (may cause blockers, and aldosterone
aorto-enteric fistula) antagonists (associated with GI
■ Renaldisease,aorticstenosis,or bleeding)
hereditary hemorrhagic ■ Bismuthandironcancauseblack
telangiectasia (may cause stools and alter clinical presentation
angiodysplasia) → If insturcting on occult
■ Helicobacter pylori (H. pylori) blood test, they need to
infection or smoking (can lead to hold bismuth and iron
peptic ulcer disease) ○ Patient symptoms can vary due to the
■ Smoking, alcohol abuse, or H. severity of blood loss. Symptoms include:
pyloriinfection(mayincreaseriskof dizziness, lightheadedness, confusion,
GI malignancy) angina,severepalpitations,andcold/clammy
■ Hospitalizationforalife-threatening extremities, upper abdominal pain,
critical illness (may cause stress gastroesophagealreflux,dysphagia,nausea,
ulcers, especially in patients with emesis, jaundice, abdominal distension
respiratory failure) (ascites), involuntary weight loss, cachexia.
■ Vomiting, straining with stool or ○ Physicalexaminationandassessmentfor
lifting, or severe coughing (may hemodynamic instability and hypovolemia
precipitateMallory Weiss tear) ■ Tachycardia indicates 15% of total
→ MalloryWeiisTearifdoing blood volume loss; indicates
forceful vomiting like mild-moderate hypovolemia
strainingorretching,itcan → Compensatory from
cause the layer of volume loss
esophagus to stretch and ■ Orthostatic or supine changes in
tear.Vomitingw/bleeding, blood pressure (may suggest
and also black stool form moderate to severe blood loss)
swallowing blood indicate 15% total blood volume
■ Comorbid conditions that may loss
affect management include: ■ Hypotension (suggests
→ Coronary artery disease life-threateningbloodloss)indicates
and pulmonary disease 40% of total blood volume loss
make patients susceptible → Needsimmediatemngmt-
to adverse effects of BLOOD TRANSFUSION
anemia ■ Rectal exam (to assess stoolcolor
→ Renal disease and heart [melena, hematochezia, brown])
failure predisposepatients ■ Significant abdominal tenderness
to volume overload with with signs of involuntary guarding
fluid resuscitationorblood (suggests perforation)
transfusions. ■ Signs of advanced liver disease
→ Coagulopathies, such as jaundice, ascites, and
thrombocytopenia, or liver altered mental status
dysfunction may make ○ Laboratory Tests
bleeding difficult tocontrol
20
■ ype and crossmatch if patient is
T ● inimally invasive techniques to control bleeding
M
high-risk, hemodynamically include sclerotherapy, embolization, and other
unstable, or has severe bleeding vascular occlusion techniques.
■ Type and screen for ○ Scelortherapy is like cauterization, it burns
hemodynamically stable patient out any dilated blood vessels
without signs of severe bleeding ● The 2019 International Consensus on the
■ Complete blood count Management of Patients with Nonvariceal Upper
→ Initial hemoglobin, then Gastrointestinal Bleeding recommends a transfusion
every 2 to 8 hours, threshold of 8 g/dL for allpatientsexceptthosewith
depending on severity of exsanguinating bleeding (Barkun et al., 2019). For
the bleed unstable or exsanguinating patients, see the table
→ Note excessive crystalloid below:
administrationcancausea ○ Hemodynamically Unstable Patients
falsely low hemoglobin ■ Admit patients with hemodynamic
value instability or active bleeding to
■ Serum electrolytes intensive care forresuscitationand
■ Liver enzymes (AST, ALT) vital sign monitoring.
■ Coagulation studies ■ For patients with active bleeding,
■ Ratio of blood urea nitrogen to begin fluid resuscitation
serum creatinine greater than 30 immediately; administer 500 mL of
■ Serial electrocardiogram and normal saline or lactated Ringer’s
cardiac enzymes may beindicated solution (plasma expanders) over
in patients at risk for demand 30 minutes.
ischemia or myocardial infarction ■ Administer blood products, as
■ Check stool for occult blood recommended in the table below.
○ Nasogastric lavagemaybehelpfulifsource ■ Avoid over-transfusion in patients
of bleeding is unclear or to clean stomach withsuspectedvaricealbleedingas
prior to endoscopy. If esophagogastric it can worsen the condition.
varices are suspected, place gastric tubes
only at discretion of gastroenterologist.
○ Problems with hemodynamic so need rapid
assessment in ABC, also reference it to
Maslow’s Hierarchy of Needs
○ Ifstabilized,assessseverityofbleedingand
idenify the cause if upper or lower and
determine underlying conditions that may
affect the management
Management
○ or stable patients with hemoglobin less
F
than7g/dL(70g/L),ifbleedinghasstopped,
● ssessment and reassessment of airway, breathing,
A
the recommendation is to transfuse 1 unit
circulation and hemodynamics
PRBCs, with secondunitavailable(Stanley,
● Closely monitor airway, vital signs, cardiac rhythm,
2019).
urine output, nasogastric tube output (if nasogastric
tube in place) and overall clinical status.
Medications
○ If hemodynamically unstable and doing
transfusion, can cause poor urine output,
● or all patients with suspected or known severe
F
also with gastric lavage
bleeding:
○ Include GCS
○ Proton pump inhibitors
● Keep patient NPO.
■ Evidence of active bleeding (i.e.,
● Provide supplemental oxygen.
hematemesis, hemodynamic
● Continuously monitor pulse oximetry.
instability): give esomeprazole or
● Obtain intravenous (IV) access with either two 18
pantoprazole, 80 mg IV and start
gauge or larger IV catheters and/or large bore,
pantoprazole infusion at 8 mg/hr
single-lumen central lines.
■ If no evidence of active bleeding,
○ G18 for crystalloids
still give PPI but lower dosage:40
● Obtain immediate consultation with
mg IV every 2 hours
gastroenterologist.
● For patients with known or suspected
● Obtain advanced imaging as necessary such asCT
esophagogastric variceal bleeding and/or cirrhosis:
angiogram to assess for active site of bleeding
○ Administer somatostatin or its analogue,
● Volume resuscitation with packed red blood cells
octreotide(Bajaj & Sanyal, 2022)
● Reversal of any coagulopathies or use of
■ Octreotide 50 mcg IV bolus
anticoagulants
followed by continuous infusion at
● Trend hemoglobin and hematocrit
50mcg/hour;notrecommendedin
● Consult with surgical and interventional radiology:
patients with acute nonvariceal
○ If endoscopic therapy will not be successful
UGIB
○ If patient is at high risk for rebleeding or
■ Treatmentcontinuesfor3to5days
complications associated with endoscopy
following cessation of bleeding
○ If patient may have an aorto-enteric fistula
21
○ dminister antibiotics (i.e., ceftriaxone or
A ■ imilar to hemorrhoidal banding;
S
fluoroquinolone) for Spontaneous Bacterial small elastic bands are placed
Peritonitis (SBP) prophylaxis aroundvaricesinthedistal5cmof
● Anticoagulants and antiplatelet agent the esophagus
considerations ● Endoscopic sclerotherapy (ES)
○ Current daily use should not delay ○ Injection of sclerosant solution into the
endoscopy varices using an injection needle that is
○ Should be held in patients withGIbleeding passedthroughtheaccessorychannelofthe
until source is identified endoscope
○ Consider reversal agents (i.e., prothrombin ○ Same as cryotherapy, it enhances and
complex, vitamin K), however risk of causes it to “nasusunog” resulting to
reversing anticoagulation (such as stroke) shrinkage. Used in px with spider veins.
should be weighed against risk of bleeding Common treatment in varcosiities
without reversal ○ Potential complications
■ Local: ulceration, bleeding,
Endoscopy dysmotility, stricture formation, and
portal hypertensive gastropathy
● pperendoscopyisthefirstchoiceforacuteupper
U ■ Regional: esophageal perforation
GIbleedingandhasahighsensitivityforlocatingand and mediastinitis
identifying bleeding lesions in the upper GI tract. ■ Systemic: sepsis and aspiration
● Once identified, therapeutic endoscopy can achieve with ventilation/perfusion mismatch
acute hemostasis and prevent recurrent bleeding. and hypoxemia
● Early endoscopy (within 24 hours) is recommended
for most patients with acute UGIB. Balloon Tamponade
● For patients with suspected variceal bleeding,
endoscopy should be performed within 12 hours of ● alloon tamponade may be performed as a
B
presentation. temporary measure for patients with uncontrollable
● The patient should be adequately resuscitated and hemorrhage due to varices while a definitive
stabilized prior to endoscopy. treatment is being arranged.
○ If there is activebleedingandendoscopyis ○ Devices for balloon tamponade include
done, it can cause pulmonary aspiration, Sengstaken-Blakemore tube, Minnesota
also adverse effect on sedation, GI tube, and the Linton-Nachlas tube.
perforation, or increase bleeding during ○ Endotracheal intubation is necessary when
procedure using these devices to prevent aspiration.
● Risks include: ■ After intubation, balloon is inflated.
○ Pulmonary aspiration Applies pressure to bleeding
○ Adverse reactions to conscious sedation causing minimal bleeding
medications ○ Equipment includes a tamponade tube kit
○ GI perforation (tube and clamps), a manometer (not
○ Increased bleeding during the procedure needed for Linton tubes), large-volume
● GI barium studies are contraindicated in acute syringes, traction/pulley system to maintain
UGIB as they will interfere with endoscopy, constant tension on thetube,andadequate
angiography, or surgery. suction.
● Factors Associated with Rebleeding ○ Before tube placement, inflate the balloons
○ Hemodynamic instability (systolic blood with air and hold underwater to assess for
pressure less than 100 mmHg, heart rate leakage.
greater than 100 beats per minute) ○ Placepatientinsupineorleft-lateralposition,
○ Hemoglobin less than 10 g/L lubricate tube and insert through mouth or
○ Active bleeding at the time of endoscopy nostril until at least 50 cm of the tube has
○ Large ulcer size (greater than 1 to 3 cm) been advanced.
○ Ulcer location (posterior duodenal bulb or ○ Ports are suctioned to remove all air and
high lesser gastric curvature) thengastricballoonisinflatedwith100mLof
ndoscopy Therapy
E air.
○ Radiograph should be obtained to confirm
● For bleeding peptic ulcers placement below the diaphragm priortofull
○ Local injection of epinephrine inflation to avoid esophageal rupture; once
■ Ephinephrine can cause confirmed, the balloon can be filled withan
vasoconstriction that minimizesthe additional 350 to 400 mL ofair,thenclamp
bleeding the air inlet.
○ Clipping of actively bleeding ulcers or ○ Thetubeispulleduntilresistanceisfelt;the
Mallory-Weiss tears tube is then securely fastened to a pulley
○ Thermal probe coagulation, often in device or taped to a football helmet to
conjunction with epinephrine injection maintain tension.
■ Same as cauterization, causing ○ If bleeding continues after inflation of the
shrinkage and results to minimal gastric balloon, the esophageal ballooncan
bleeding be inflated 30to45mmHg;pressureofthis
● For bleeding esophageal varices: balloon should be checked at least hourly.
○ Endoscopic variceal ligation (EVL) is the
initial treatment of choice.
22
○ onotoverinflatetheesophagealballoonas
D t hyroidhormones,resultinginenlargement
this can cause esophageal necrosis or of the gland (goiter).
rupture. ○ Inhibits the upload of iodine in the system
○ Once bleeding is controlled,pressureinthe ■ Bok choy
esophageal balloon can be reduced by 5 ■ Broccoli
mmHg to goal pressure of 25 mmHg. ■ Brussels sprouts
○ Tubecanbeleftinplacefor24to48hours; ■ Cabbage
the gastric and esophageal balloonsshould ■ Cauli flower
be deflated every 12 hours to check for ■ Horseradish
rebleeding. ■ Kale
○ There is a high riskforrebleedingfollowing ● Take Iodine- seafood and iodize salt
balloon deflation.
○ Use with caution inpatientswithrespiratory Hyperthyroidism
failure, cardiac arrhythmias, or hiatal hernia.
● Cause:
Uncontrolled Bleeding ○ Primary
■ Autoimmune Disease
● assive uncontrolled upperGIbleedingisamedical
M ■ (Grave’s Disease)
emergency. ■ ↑TSAb mimics TSH
● All bedside caregivers should wear full personal ■ ↑thyroid hormones
protective gear, including eye protection. ○ Secondary
○ To protect from blood-borne disease ■ Pituitary Tumor
● Immediateprioritiesincludecontrollingtheairwayand → Increases TSH and TH
balancing resuscitation with blood products in more than the required
hemodynamically unstable patients. number
● Reverse any anticoagulants the patient has been ■ ↑TSH, ↑TH
taking. ● Diagnosis:
● Give fresh frozen plasma to patients with known or ○ Radioactive Iodine uptake (↑35% uptake)
presumed coagulopathy. ■ LOW DOSE DIAGNOSIS
● For esophageal varices, if bleeding cannot be ■ Measures thyroid gland absorption
controlled endoscopically, treatment options include rate
transjugular intrahepatic portosystemic shunt (TIPS) ■ Capsule is given and is measured
placement or surgical shunting. 2, 6, 24 hours after
● As a last resort, resuscitative endovascular balloon ■ Normal value: 5%-35% in 24 hours
occlusion of the aorta (REBOA)canbeusedtolimit ■ Decreased absorption: ↓5%
blood loss and supportperfusionofvitalorgansuntil hypothyroid
bleeding sources can be directly controlled. ■ Increased absorption: ↑35%
hyperthyroid
I. THYROID GLAND DISORDERS ■ Avoid contact with feces and urine
● oiter
G (flush toilet 2-3x)
● Hyperthroidism → Elimination is via urine or
● Hypothroidism feces
■ Followed by thyroid scan
Goiter (Enlarged Thyroid) ○ Thyroid Scan (hot spot, toxic nodulargoiter
TNG)
● Cause: ■ Detects activity of the nodes
○ Iodine Deficient (↓40 fg/day of iodine) ■ Administered after RAIU
○ Hypothyroidism (compensatory enlargement) ■ Can detect activity of the nodes.
○ Hyperthyroidism (hypertrophy) ○ ↑PBI, ↑T3, ↑T4, ↑FT4 thyroxine free
○ CA of thyroid ○ Exophthalmos
● Diagnosis: ■ Classic sign of Grave’s disease
○ History and PE (I,P,A) ■ Irreversible
○ Blood Exam (T3 and T4, TSH) ■ Provide eye care: artificial tears,
○ Imaging (Thyroid Scan) ■ Cover with moistened gauze or
○ FNAB (fine needle aspiration biopsy) tape the eyelid at night,
● S/Sx: ■ Elevate head, dark glasses at
○ Enlargement (visible) daytime,
○ May lead to tracheal obstruction → Difficulty in vision
■ Difficulty breathing and swallowing ● S/Sx:
from pressure on trachea ○ ↑BMR
○ Maybe hyperthyroid or hypothyroid s/sx ○ Brain - inability to concentrate
● Intervention: ○ Eyes - exophthalmos
○ Prevention(eatseafoods,avoidgoitrogenic ○ Heart - ↑HR
foods) ○ Blood vessels - constrict, ↑BP
○ Thyroidectomy ○ Lungs - ↑RR
● Avoid Goitrogenic ○ GIT - diarrhea
○ Goitrogens - Are foods that can affect ○ ↑ Body temp - heat intolerance
thyroid function by inhibiting synthesis of ○ Gonads - metrorrhagia to amenorrhea
○ Weight loss
23
○ hyroid Storm!!!
T (↓T3, T4, ↑TSH)
■
○ Thyroid Storm, Crisis, Thyrotoxicosis ■ Thyroidectomy
■ Triggered by: ○ Secondary
→ Over palpation of thyroid ■ Hypophysectomy
gland ■ (↓TSH, ↓T3, T4)
→ Post op thyroidectomy ● Diagnosis:
(within 24H) ○ Radioactive Iodine uptake (↓5% uptake)
→ Too much stress ○ Thyroid Scan (cold spot, non toxic nodular
■ S/Sx: goiter [NTNG])
→ ↑ Body temp.-early sign ○ ↓ Protein Bound Iodine, ↓ T3, ↓ T4,
→ Cardiac arrhtyhmias ○ ↓ FT4 thyroxine free
■ ER situation! ● S/Sx:
■ Give: antithyroid, betablockers ○ ↓BMR
● Management: ○ Brain-slow
○ Symptomatic ○ Eyes-puffiness
■ Increased body temp - manipulate ○ Heart- ↓ HR
environment, fluid intake, TSB ○ Blood vessels-dilate, ↓ BP,
○ Anti-thyroid Drugs ○ Atherosclerosis
○ Radioactive Iodine (high) ○ Lungs - ↓ RR, CO2 Narcosis
○ Surgical Thyroidectomy ○ GIT - constipation
○ Prevent Thyroid Crisis ○ ↓ Body temp - cold intolerance
● Ani-thyroid drugs ○ Gonads - menorrhagia to Amenorrhea
○ Thionamides (Propylthiouracil) ○ Weight gain
○ Methimazole (Tapazole), Carbimazole ○ Myxedema Coma!!!
○ Lifetime meds, 3x/day ■ Triggered by:
○ Side Effects: → Post op thyroidectomy
■ Agranulocytosis (report sore throat) (24H after)
■ Liver disease (jaundice, abd’l pain) → Following radiation
● Radioactive Iodine treatment
○ HIGH DOSE TREATMENT → Too much stress
○ 123-I or 131-I (series) → Hypothermia
○ Action: destroys thyroid tissue ■ S/SX:
■ Minimizes function of organ → ↓LOC - early sign - coma
○ Disadvantage: complete destruction ■ ER situation!
○ Avoid contact with feces and urine (flush ■ Give: thyroid hormones
toilet 2-3x) ● Management:
○ Private room, single bathroom (2-5 days) ○ Symptomatic
● Surgical Thyroidectomy ○ Life time supplement of synthetic T3 and T4
○ SSKI Saturated Solution of Potassium ○ Prevent Myxedema Coma
Iodide (Lugols) ○ Synthetic Thyroid Hormones
○ Is given preop to reduce thyroid vascularity ■ Lifetime meds, OD, am, b4
and bleeding breakfast, empty stomach
■ Thyroid gland is vascular, to ■ T4 Synthroid, Levothyroid
minimize bleeding tendency ■ T3 Cytomel
○ Givenwithjuicetodisguisetaste,given with ■ T3 & T4 Proloid
straw to prevent staining of teeth ■ Side Effect: adrenal insufficiency,
○ Post-op Thyroidectomy: hyperthyroid
■ Position: SUPINE or SEMI
FOWLERS, no hyperflexion and
hyperextension of the neck
■ Check stridor/crowing – upper
airway obstruction – insert TT
→ Also check drainage
■ Check back and side - bleeding
■ Check for Trousseau/chvostek –
Tetany – give Ca Gluconate
■ Check Hoarseness - laryngeal
nerve damage if it persisits aftera
week
■ Watch out thyroid crisis within 24
hours
Hypothroidism
● Cause:
○ Primary
■ Autoimmune Disease
■ (Hashimoto’s Thyroiditis) J. THYROID EMERGENCIES
■ ↑TMAb – destroys thyroid gland
24
● rompt recognition of thyroid emergencies is critical
P
■ eat intolerance
H
to decrease complications and mortality. ■ Tremors
● Management requires both medical and supportive ■ Palpitations
treatment provided in the critical care setting. ■ Tachycardia
■ Weight loss
Myxedema Coma ■ Hyperreflexia
■ Warm and moist skin
● yxedema coma is a severe, life-threatening
M ■ Menstrual abnormalities
emergencythatcanoccurinlong-standing,untreated ■ The following life-threatening signs
hypothyroidism. Diagnosis is based on clinical may also be present:
manifestations such as altered mental status and → Hyperpyrexia (fever
hypoventilationassociatedwithslowingoffunctionsof greater than 106 degrees
multiple organs, along with laboratory results Farhrenheit)
consistent with hypothyroidism. Treatmentshouldbe → Congestive heart failure
started promptly given the increased risk of mortality. → Vomiting
● Signs and Symptoms: → Impaired mental status
○ Extreme lethargy and diminished mental ● Treatment of Thyroid Storm
status -Lethargic ○ Beta-blocker to control heart rate
○ Hypothermia ○ Methimazole or propylthiouracil todecrease
○ Hypotension production of thyroid hormone
○ Hypoventilation ○ Iodine solution to inhibit thyroid hormone
○ Hypercapnia release
○ Hypoglycemia ○ Glucocorticoids to decrease the conversion
○ Hyponatremia of T4 to T3
○ Bradycardia ○ Supportive measures include:
○ Pericardial effusion ■ IV fluids
● Treatment of Myxedema Coma ■ Oxygen
○ ThyroidhormonereplacementwithT4and/or ■ Cooling
T3, usually intravenous (IV) ■ Treatment of any precipitating
○ Glucocorticoids, until coexisting adrenal causes
insufficiency is ruled out ○ Plasmapheresis when traditional therapy is
○ IV fluids for electrolyte replacement unsuccessful
○ Warming blankets ● Nursing Considerations
○ Supportive care including mechanical ○ Thyroid storm can occur in patients with or
ventilation as required without preexisting hyperthyroidism.
● Nursing Considerations ○ Patients with knownseverehyperthyroidism
○ IV hormone replacement should be who are noncompliant with prescribed
administered only as IV push through a antithyroid medications maydevelopthyroid
syringe, rather than through infusion tubing storm.
due to high concentrations lost from
adherence to polypropylene tubing. ALTERED NEUROLOGIC FUNCTION
○ Improvements in serum T3 and T4
concentrations may be seen before the A. CVA
normalization of serumTSHconcentrations,
● Interconnected with a lot of complications: HPN, DM
and serum thyroid function tests should be ● IncreasingbecauseifyouhaveDM,heartprobs,you
obtained every one to two days during are at risk of developing this disease
treatment.
○ Improvements in clinical cardiovascular, Types of Stroke
renal, pulmonary, andmetabolicparameters
may take as long as a week. ● INFARCT: Blockage of Artery
○ Thrombotic
Thyroid Storm ○ Embolic
● pposite of Myxedema Coma
O ISCHEMIC STROKE
● Thyroid storm refers to elevated thyroid hormone ● isruption of the blood supply due to an
D
concentrations; thyroid stormisararediagnosisand obstruction, usually a thrombus or embolism, that
results from untreated hyperthyroidism, abrupt causes infarction of brain tissue
cessation of antithyroid medication, or from ● Anyobstructionofbloodflowgoingtoyourbrainthat
thyroid or nonthyroid surgery, trauma, infection, can be caused by thrombus or emboli
or an acute iodineload.Diagnosisofthyroidstorm ● Once it is dislodged and went to cerebrovascular
ismadeusingbiochemicallaboratorytestsconfirming vessels causing blockage,theareahasnoperfusion
thyrotoxicosis in a patient displaying the severe, so the area is at risk for infarction
life-threatening symptoms of hyperthyroidism.
● Signs and Symptoms of Thyroid Storm Causes of Ischemic Stroke
○ Clinical manifestations include exaggeration
of common hyperthyroid symptoms:
● uildup of fatty deposits in the arteries of the neck
B
■ Anxiety ● Heart conditions that lead to clot formation (e.g. AF)
■ Fatigue ● Blood condition that promote clotting
■ Diaphoresis
25
Non-Modifiable Risk Factors
● olden hour in stroke:3 HOURS
G
● If you detect early stage, most likely stroke can be
● troke is Preventable
S prevented
● Relative Risk: ● SUDDEN....
○ Age ○ weakness on one side of the body
■ Doubles per decade after age 55 ○ numbness/tingling in the face/arm/leg
■ Habang tumatanda mas at risk ka ○ loss of speech or trouble understanding
○ Gender speech
■ Males > Females ○ slurring of speech
○ Previous stroke ○ loss of vision, particularly on one eye or
■ 10x of getting it again double vision
○ Race-ethnicity ○ severe and unusual headache
■ Blacks > Whites ○ dizziness and loss of balance
○ Heredity ● If you are atriskandexperiencingthese,checkwith
■ IfthereishistoryofDM,CAD,HPN, your doctor
most likely you are at risk
odifiable Risk Factors
M Delivery: Prehospital Transport and Management
● ypertension
H ● Cincinnati Prehospital Stroke Scale
● Cigarette smoking ○ Facial Droop (show teeth or smile)
● Alcoholism ○ Arm Drift (close eyes and hold both arms
● Diabetes out)
● Heart disease ○ Speech (repeat "you can'tteachanolddog
● Hypercholesterolemia new tricks") or simply as their name
● Heavy alcohol intake ○ Also T for Time
● Obesity ■ Time 0 - time where manifestation
● Physical inactivity / Sedentary lifestyle started
● Stress ■ Check the last time when pt was
● Heavy snoring normal
○ Because of depletion of oxygen going inside ○ Score each as either normal or abnormal,
anifestations
M compare sides when appropriate.
● Kalaban sa stroke is ORAS
● eypoint: disruption ofperfusionleads to infarction
K
● Symptoms depend upon thelocationandsizeofthe Differentiating Ischemic from Hemorrhagic Stroke
affected area
● Numbness or weakness of face, arm, or leg, ● Gold standard isplain CT scan
especially on one side ○ Hyperdense (bright) lesion - bleed or
● Confusion or change in mental status intracerebral hemorrhage (ICH)
● Trouble speaking or understanding speech ○ Normal/Clear - acute infarction ortransient
● Difficulty in walking, dizziness, or loss of balance or ischemic attack (TIA)
coordination ○ Hypodense(dark) - infarction
● Sudden, severe headache ● Visualize the stroke to differentiate
● Perceptual disturbances
Type of Stroke: Use of Brain Imaging
● Computed Tomography
○ Widely available, relatively inexpensive,
Aphasia non-invasive, and quick
○ Accurately differentiate hemorrhagic and
● LUENT - retains verbal fluency but may have
F ischemic stroke
difficulty in understanding speech ○ Should be performed and interpreted ASAP
● WERNICKES-abletospeakbutlacksclearcontent,
● Lead the team in understanding what is happening
information, and direction, with difficulty with ● Dark areas show area of infarction
comprehension
● BROCAS - partial or complete inability to initiate
speech, form words and word finding
● ANOMIC/AMNESIAC - speechisalmostnormal,but
marred by word finding difficulty
● CONDUCTION-comprehensionoflanguageisgood
but has difficulty repeating spoken material
● NON-FLUENT - speech is sparse and produced
slowly and with effort and poor articulation; usually
has a relatively preservation of auditory
comprehension
● GLOBAL - severe disruption of all aspects of
communication
Detection: Early Recognition of Warning Signs ● Magnetic Resonance Imaging
○ More expensive and less widely available
26
○ Longer acquisition time compared to CT - therapy for blood pressure control
ifficult in uncooperative patients
d should be deferred unless there is:
○ Contraindicated in patients with metallic → Left ventricular failure
implants (e.g. IOL, pacemaker) → Aortic dissection, or
○ More sensitive in detecting small lesions → Acute myocardial ischemia
○ Can detectlesionsasearlyas6hoursfrom → Renal failuresecondaryto
onset of stroke (as early as 90 minutes for accelerated HTN
Diffusion MRI) → Hemorrhagic
transformation
Severity of Stroke → Because there may be
sudden drop in BP
● NIH Stroke Scale → Mahirap imanage if
○ 1. Level of consciousness masyadong bagsak
○ 2. Speech and Language ■ Patients who are potential
○ 3. Visual assessment candidates for rTPA therapy but
○ 4. Motor function who have persistent elevations in
○ 5. Sensation and neglect SBP >185 mmHg or DBP >110
○ 6. Cerebellar function mmHg may be treated with small
● Hunt and Hess Scale for SAH doses of IV anti-hypertensive
○ Grade 1 Asymptomatic medication to maintain the BP just
○ Grade2Severeheadacheornuchalrigidity, below these limits:
no deficit → Maintain MAP of 100-130
○ Grade 3 Drowsy, minimal neurological deficit → Avoiddrops>20%ofinitial
○ Grade 4 Stuporous, moderate to severe MAP
hemiparesis → Acute ischemic stroke
○ Grade 5 Deep coma, decerebrate posturing need perfusion =
circulation. Don’t want
Decision: Stroke Therapies circulation to go low, so
maintain MAP
● General Management of Acute Stroke
○ Management of seizures
○ IV fluids ○ Management of increased ICP
■ Avoid D5W and overloading ■ Hyperventilation: PaCO2 = 25-30
○ Blood sugar mm Hg
■ Determine immediately ■ Mannitol: 0.5 - 2 g/kg/dose
■ D50 if low; insulin if >300 mg/dl → Make sure BUNandCrea
○ Thiamine 100 mg are normal because it
■ If malnourished, alcoholic might cause acute kidney
○ Oxygen injury
■ Pulse ox; give if indicated ■ Neurosurgical decompression
■ Aid in brain for perfusion
○ Acetaminophen Specific Management
■ If febrile
○ NPO
● reatment option: Admit to stroke unit
T
■ If at risk for aspiration ● Anti-occlusives
○ Management of elevated blood pressure ○ Thrombolytic therapy (r-TPA) within 3 hours
■ Based on mean arterial pressure ■ Give accordingly to time
(MAP) ■ Promising given therearenoother
■ Check commoncausesofelevated comorbidities
BP: full bladder, pain, trauma, ○ Anti-platelets (ASA, Clopidogrel) within 48
increased ICP hours
■ Parenteraldrugsmaybewarranted ○ Anticoagulant (Warfarin, LMWH) within 48
in the ff conditions: acute MI, left hours
ventricular failure, aortic dissection ● Neuroprotectants
■ Avoid the use of sublingual ○ Avoid hypotension, hypoxemia,
nifedipine which can result in hyperglycemia, hyponatremia, fever
precipitous decline in BP ○ “Neuroprotectant drugs"
■ How to get MAP: 1 Systolic + 2 ● Hemicraniectomy (last option)
Diastolic / 3
■ For SBP>220, DBP 121-140, Neuroprotection
MAP>130: titratable antiHPN meds
→ Can taper the doseeasily ● AVOID the Following:
once effects are achieved ○ Hypotension (Rx only if MAP >130 mm Hg)
■ For DBP>140: IV infusion of ■ Affects perfusion
antiHPN agent ○ Hypoxemia
■ SBP between 185-220, DBP ○ Hyperglycemia
105-120: not treated except in ○ Hyponatremia
specific conditions ○ Fever
■ IfSBPis185-220mmHgorDBPis
105-120 mmHg, emergency Nursing Interventions
27
■ egular turning and positioning
R
● nsure patent airway
E ■ Keep skin dry and massage
● Keep patient on LATERAL position NON-reddened areas
● Monitor V/S and GCS, pupil size ■ Provide adequate nutrition
● IVF is ordered but given with caution as not to
increase ICP HEMORRHAGIC STROKE
● NGT inserted ● Rupture of an artery
● Medications:Steroids,Mannitol(todecreaseedema), ○ Intracerebral
Diazepam ○ Subarachnoid
● Hospital Setting: ● Caused by bleeding into brain tissue, theventricles,
○ Improve Mobility and prevent joint or subarachnoid space
deformities ○ Monroe Kelly Hypothesis: Any
■ Correctlypositionpatienttoprevent disquelibrium among the three can cause
contractures increasing ICP
→ Place pillow under axilla ■ CSF, Blood, and Brain Tissue
→ Hand is placed in slight ○ E.g. Ischemic stroke there isblockagefrom
supination - "C" thrombus/embolus, there is increased ICP
→ Change position every2 because of alteration in flow
hours ● May be duetospontaneousruptureofsmallvessels
○ Enhance self-care primarily related to hypertension; subarachnoid
■ Carry out activities on the hemorrhage due to a ruptured aneurysm; or
unaffected side intracerebral hemorrhage related to amyloid
■ Prevent unilateral neglect - place angiopathy, arterial venous malformations (AVMs),
some items on the affected side!!! intracranial aneurysms, or medications such as
■ Keep environment organized anticoagulants
■ Use large mirror
● Brain metabolism is disrupted by exposure to blood
○ Manage sensory-perceptual difficulties ● ICP increases due to blood in the subarachnoid space
■ Approach patient on the ○ Brian compression follows
unaffected side ○ Pressure finds it way to be lowered
■ Encourage to turn the head to the ○ Danger is brainstem compression, a lot of
affected side to compensate for vital functions begin to weaken, disappear
visual loss and be disrupted
○ Manage dysphagia ● Compression or secondary ischemia from reduced
■ Place food on theUNAFFECTED perfusion and vasoconstriction injures brain tissue
side
■ Provide smaller bolus of food Manifestations
■ Manage tube feedings if prescribed
■ Put pt in strict aspiration precaution
● imilar to ischemic stroke
S
○ Help patient attain bowel and bladder control ● Severe headache
■ Intermittent catheterization is ● Early and sudden changes in LOC
done in the acute stage ● Vomiting
■ Offer bedpan on a regular schedule
■ High fiber diet and prescribed
fluid intake
■ Don’t want any pressure that may Transient Ischemic Attack
increase CP
■ Valsalva manuever can cause IICP ● hereisresolution,fastestiswithinanhourupto24
T
○ Improve thought processes hours
■ Support patient and capitalize on ● Example: Slurring of speech, after meds it will be
the remaining strengths resolved and then there is no brain injury
■ Rehab starting from PROM ● In stroke, same manifestation but there is INJURY.
exercise The resolution is with 24 hours
○ Improve communication
■ Anticipate the needs of the patient Additional Notes
■ Offer support
■ Provide time to complete the ● hen pt has AF, the propensity to develop clots is
W
sentence high because during fibrillation, the heart does not
■ Provideawrittencopyofscheduled contract,bloodmovesslowyly,thereisstasiscausing
activities clots.Whentheclotsbecomeembolusandlodgeinto
■ Use of communication board the brain, this results tocardioembolic stroke.
■ Give one instruction at a time ● StroketoavoidcomplicationofDVT.Toavoidthis,we
■ On psychological aspect, the pt is can let them wear anti-embolic/compression
adjusting. There are episodes of stockings, or refer to rehabilitation for exercises.
denial and depression because ● Patient with altered tissue perfusion, ensure that
there is total adjustment in the ADL circulation will not be aggravated by any for of
○ Maintain skin integrity obstruction such as neck flexion or head flexion.
■ Use of specialty bed (air Advisable for 30-45 degree angle position
compression mattress) (semi-fowler)
→ CHECK Bed Sore Protocol
28
● onitoring vital signs check for thebloodpressure.
M ● CIRCULATORY/ DISTRIBUTIVE
Compute for the MAP, to check for the perfusion. ○ SEPTIC
Doctor will tell the target MAP. ■ Resultsfromaccumulationoftoxins
○ Example: MAP is 80-90 - BP is 130/90. and bacteria in the blood
■ 130 + (2x90) / 3 = 103 ○ NEUROGENIC
○ IfoutsideMAP,refertodetermineifweneed ■ brain hypoxia in origin
to give antiHPN meds, check for pain, or ○ ANAPHYLACTIC
repositioning ■ caused by toxic allergic reaction
● NEURO VITAL SIGNS IS IMPORTANT
○ GCS, Usual vital signs, NIHSS* (possible),
Pupillary response A. HYPOVOLEMIA
● Assess for anything that cause IICP
● ain problem is bleeding
M
○ Bladder distention - catheter ● Volume is lost
○ Abdominal distention - given Lactulose ○ #1 Management - FLUIDS
● Turning to prevent complication fromimmobility(e.g.
bed sores, pneumonia)
● Aspiration Precaution: If in NGT, check placement,
position semi-fowler
● Communication: If can’t move, can’t write - Picture
board. But if can write - give pen and paper
○ Prevent unilateral neglect - put objects on
the affected/paralyzed side
● Help in performing ADLs
● Stroke is preventable in a certain period, but once
ischemia sets in it, isIRREVERSIBLE
○ Rehabilitation is important
○ Lifestyle changes
SHOCK
SIRS/ Sepsis/ Septic Shock
● IRS-Nofocusyet.Responseissytemic/genericbut
S
leaning toward infection
● Sepsis - it is defined/focused. There is beginning
organ affectation
● Septic shock - severity to beginning organ failure.
Comes from primary sepsis
● Roleofshockistoknowtheunderlyingcause.Unless
you find, you cannot reverse the effect
● Understant the management to the immunesystem.
Always consider age
● Central Venous Pressure -Centrallineisinsertedto
measure. Used as parameter for perfusion and to
check if diuretics cause
Classes of Hypovolemic Shock
TYPES OF SHOCK
● t the end of the a spectrum of disease, one
A
complication is Shock
● Compensatory mechanism - the body will try to
compensate
● Progressive/Irrevirsible stage - affects the entire
system defining it as multi-organ failure
● Types of Shock
○ Hypovolemic (fluids)
○ Cardiogenic (pump)
○ Redistributive (pipes)
■ Septic, Neurogenic , Anaphylactic
● HYPOVOLEMIC
○ Significantfluidlossfromintravascularspace
may be due to hemorrhage, burns, G.I
losses, fluid shift Clinical Signs of Acute Hemorrhagic Shock
● CARDIOGENIC
○ Pump failure mechanism most common ● Signs are from compensatory mechanisms
cause is M.I
○ Any restriction of cardiacperfusionwilllead
% Blood Loss Clinical Signs
to cardiogenic shock
29
● loodTransfusion-WholeBloodorPRBC,andother
B
<15 Slightly increased heart rate components missing
15 - 30 Increase HR, decreased CARDIOGENIC SHOCK
DBP (narrow pulse ● Mechanism
pressure), prolonged ○ Defect in cardiac function (lost > 40% Fxn)
capillary refill, flat neck veins ● Signs
○ Decreased cardiac output
30 - 50 bove
A findings plus ○ Increased PAOP/CVP
hypotensions, confusion, ○ Increased SVR
acidosis, decreased urine ○ Decreased left ventricular stroke work
output (LVSW)
● Problems is contractility = Improve contractility
> 50 efractory
R hypotension,
refractory acidosis, death
Treatment
● everse hypovolemia & hemorrhage control
R
● Crystalloid vs. Colloid
○ 1 L crystalloid = 250 ml colloid
■ Watch for fluid overload by
reassessing lung sounds
■ 3:1Rule(3cccrystalloidfor1ccbld
loss)
■ Watchforhyperchloremicmetabolic
acidosis when large volumes of
NaCl are infused
■ Best to give in 250 mL boluses in
CHF followed by reassessment for
another 250 cc bolus
● Colloids: (ex: albumin)
○ Will increase osmotic pressure, watch for Symptoms
pulm edema
○ Remain in vascular space longer (several ● Skin
hrs) ○ rogressive peripheral vasoconstriction
P
○ NOT increase survival results in cool, moist, pale skin with mottling
● PRBC sooner than later ● Congestive Heart Failure Signs
○ 500 ml whole blood increases Hct 2-3%, ○ Jugular venous distenction, Hepatojugular
250ml PRBC's increases Hct 3-4% reflux, APE, Pedal edema
Increases oxygen carrying capacity ● Heart
○ Used with acute hemorrhaging (mntn Hct ○ Sounds:d/tenlargementandcongestionyou
24% and Hgb 8g/dL) can hear murmurs or S3 or S4
● NOT FOR VOLUME ○ Pulse: rapid rate and thready/weak pulse
○ FFP for coagulopathy (all factors) ○ BP: decreased BP and MAP
○ Factor vii ● Urine Output: decreases early d/t decreased renal
○ PLT for thrombocytopenia perfusion
● Pressors ● WhatyouseeinMI,youwillseeincardiogenicshock
but this is progressive
● Assess for
ppropriate Minimal Infusion Rate of Normal Saline or
A
○ Signs of heart failure
Ringer’s Lactate
○ Signs of tamponade
○ Cardiac dysrrhythmia
IV Catheter Size ravity
G 80 on P
ressure 300 ○ Myocardial infarction
height mmHg ■ Tachycardia
■ Muffled heart sounds orthirdheart
18g IV 30 - 60 ml/min 120 - 180 ml/min sound
■ Engorged neck veins with
16g IV 90 - 125 ml/min 200 - 250 ml/min hypotension
■ Dyspnea
14g IV 125 - 160 ml/min 250 - 300 ml/min ■ Edema in feet and ankles
8.5 Fr 200 ml/min 400 - 500 ml/min Treatment
● Increase oxygen supply to the heart
● ule of thumb: Crystalloid of choice - Lactated
R
○ Decrease oxygen consumption (pain
Ringer’s
meds/sedation)
○ If none, PNSS
30
○ Increase oxygen delivery (mech vent, ● Symptoms
r eperfusion of the coronary arteries) ○ Onset within seconds and progression to
● Maximize the cardiac output death in minutes
○ Maintain normal rhythm (dysrhythmics, ○ Cutaneous manifestations
pacing, cardioversion) ■ urticaria, erythema, pruritis,
○ Diastolic Vasopressors (dopamine, epi, angioedema
norepi, vasopressin) ○ Respiratory compromise
○ Improve myocardial contractility - ■ stridor, wheezing, bronchorrhea,
■ Inotropes (dobut and amrinone) resp. distress
● Decrease the afterload (workload of the LV) ○ Circulatory collapse
○ IABP ■ tachycardia, vasodilation,
○ LVAD hypotension
○ CNS
The Failing Heart ■ apprehension -> AMS-> Coma
● Improvemyocardialfunction,C.I.<3.5isariskfactor, ● Treatment
2.5 may be sufficient. ○ Remove the antigen
● Fluids first, then cautious pressors ○ ABC's
● Remember aortic DIASTOLIC pressures drives ○ IV Fluids, O2, cardiac monitor, pulse ox
coronary perfusion (DBP - PAOP = Coronary ○ First line Rx:
Perfusion Pressure) ■ Epinephrine
● Ifinotropesandvasopressorsfail,intra-aorticballoon ■ For severe bronchospasm,
pump & LV assist devices laryngeal edema, signs of upper
○ PCI - do not delay airway obstruction, respiratory
arrest or shock: IV epi
DISTRIBUTIVE SHOCK → 100 micrograms of
● It is in the peripheral area 1:100,000(place0.1mLof
● Types 1:1000 in 10 mL of NS,
○ Sepsis give over 5-10 min)
○ Anaphylactic ■ If less severe, cangive0.3-0.5mL
○ Neurogenic 1:1000 SC
● Signs ○ Second line Rx:
○ + Cardiac output ■ H1 blocker: Diphenhydramine
○ + PAOP 25-50 mg IV
○ Decreased SVR ■ H2 blocker: Ranitidine 50 mg or
Famotidine 20 mg IV.)
■ Steroids (Methylprednisolone 125
mg IV or Prednisone 40-60 mg po)
■ Albuterol
■ For patients taking Beta-blockers
with refractory hypotension, think
about glucagon
Septic Shock
● Systemic Inflammatory Response (SIRS)
○ Manifested by two or of following:
■ Temp > 38 or < 36 centigrade
■ HR > 90
■ RR > 20 or PaCO2 < 32
■ WBC > 12,000/cu mm or > 10%
Bands (immature wbc)
● Septic Shock Trail
○ SIRS → Sepsis→SevereSepsis→Septic
● asodilation can be caused by toxins, infection
V Shock
● TREAT INFECTION ○ Sepsis is the combination of the Systemic
InflammatoryResponseSyndrome(SIRS)&
Anaphylactic Shock a confirmed or presumed infectious etiology.
○ Severe Sepsis: SIRS criteria, source of
● apid onset
R infection and infection-induced organ
● Diffuse vasodilation mechanism from histamine & dysfunction or hypoperfusion abnormalities
bradykinin (sepsis + lactic acidosis/oliguria/AMS/etc.)
● Edema from increased capillary permeability ○ Septic Shock: SIRS criteria, source of
● Bronchoconstriction infection,andhypotensionnotreversedwith
○ Body reacts from a specific toxin fluidresuscitationandassociatedwithorgan
○ Body release histamine and bradykinin that dysfunction or hypoperfusion abnormalities
is aggravated by vasodilation ● Bacterial, viral, fungal infection
■ Give ANTIHISTAMINE ○ "Warm shock" is early stage
31
■ ever, tachycardia, tachypnoea,
F ○ assive venous
M pooling & arteriolar
leucocytosis, inadequate oxygen dilatation
extraction (High SVO2, Metabolic
acidosis) in infected tissues ● Signs and Symptoms:
○ "Cold shock" is late stage ○ Hypotension without tachycardia
○ Warm pink skin from cutaneous vasodilation
● Signs ○ Low BP w/ minimal response to fluids
○ E arly: warm w/vasodilation,oftenadequate ○ Accompanying Neurologic deficit
urine output, febrile, tachypneic. ● Spinal shock is not Neurogenic shock
○ Late:vasoconstriction,hypotension,oliguria, ○ Spinal Shock: the temporary loss of spinal
altered mental status. reflex activity that occurs below a total or
● Monitor findings: near total spinal cord injury
○ Early - hyperglycemia, respiratory alkylosis,
hemoconcentration,WBCtypicallynormalor ● Treatments
low. ○ Increase vascular tone and improve CO
○ Late - leukocytosis, lactic acidosis ■ Increase preload with fluids
○ Very Late - Disseminated Intravascular → CVP
Coagulation & Multi-Organ System Failure. → PAWP
■ Increase vascular tone
● Treatment → Vasopressors
○ Prompt volume replacement - fill the tank ■ Maintain heart rate
○ Early antibiotic administration - treat the → Treat bradycardia if
cause symptomatic
○ If MAP < 60 ■ Maintain adequate oxygenation
■ Dopamine = 2 - 3 μg/kg/min → WatchwithSCIbecauseof
■ Norepinephrine = titrate (1-100 thedisruptionofO2tothe
μg/min) medulla
■ Initiate therapy to prevent DVT
→ Sluggish venous flow will
increase risk factors
■ Steroids (Methylprednisolone
30mg/kg over 15 min in first hour,
then 5.4 mg/kg/hr x 23 hours)
→ There are contradicting
studies, all of which have
flaw
○ Thesymptomsofneurogenicshocktypically
last 1-3 weeks
○ Treatment is on the progressive
manifestations
● Nursing Goals
○ COMPENSATORY
■ Monitor Tissue Perfusion
■ Reduce Anxiety
■ Promote Safety
○ PROGRESSIVE
■ Prevent Complications
■ Promote Rest and Comfort
■ Support Family Members
● erform 1 hour bundle in Septic Shock
P → SupportFamilyMembers-
● Protocol - you don’t need to wait for orders support whatever decision
they have
→ Aggressive management-
Neurogenic Shock all treatment is given. Not
in DNR
● eurogenic shock has no compensatory stage
N → Conservativemanagement
● Fast progression - supportive measures.
● Essential derangement: paralysis of the sympathetic Focus only on specific
chain which controls vascular tone from injury to aspects requested by
thoracic or cervical level spinal cord injury. family
● Produces decreased SVRfromlossofvasculartone → Sometimes do Family
and bradycardia from unopposed parasympathetic Conference
input to SA node. → Determine the life goals,
● Central, Peripheral, and Sympathetic action is down the optimum quality of life
→ Organ Transplant - organ
● Caused by: that is failing, can it be
○ Spinal cord injury loss of SNS transplanted? Where is
32
y our donor? Is it going to
be rejected?
○ IRREVERSIBLE
■ Irreversible stage - only goal is
comfort and pain management
→ For the family - needs
acceptance
→ End of life care - the end
of critical care
● General Medical Management
○ 100% O2 BY NON-REBREATHER MASK
○ Intubation if O2 management is inadequate
○ Fluid resuscitation
○ Ringers Lactate is the initial fluid ofchoice.
PNSS 2nd choice Crystalloids and colloids
○ Packed RBC for massive blood loss
○ IFC insertion
○ Patient on supine position with legs elevated
○ ECG, ABG, CBC and ELECTROLYTE
○ CVP insertion
○ Main normothermia (in septic shock patient
should be kept cool bec. Fever inc.
metabolic effects of shock)
○ Vasopressors, Inotropic Agents
33
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